Jumat, 28 April 2017

best medication for asthma

best medication for asthma

for the past five to ten years, more and moreamericans suffered different kinds of allergies. for instance, allergic rhinitis, asthma orurticaria. or even anaphylactic shock. in which suddenly, a lot of histamine is releasedinto the body. and then all the blood vessels dilate. and people can just suddenly go tocoma. so we have all the medication to help the allergy symptoms. the first step is, whenyou first have allergic symptoms. you will get anti histamine medication. so that willhelp reduce your symptoms, nose congestion, itchy eyes, itchy skin. so people will stayalert, symptom free for a couple years. then the symptoms come back. so the second step,is using cortisone shots to reduce the allergy symptoms. and then the next step, we'll usethe allergy shots to desensitize the body.

but none of this treatment can eliminate allergy.so we're going to talk about how acupuncture can treat the root cause.

best inhalers

best inhalers

natural asthma inhalers: asthma mist - http://natural-asthma-inhaler.com/

best inhalers for asthma

best inhalers for asthma

remove the cap from the inhaler. remove the cap from the spacer. shake the inhaler well for 5 seconds. insert the inhaler into the open end of the chamber. ensure that the inhaler fits properly. sit-up straight or stand up. tilt your head back slightly. before starting to inhale breathe out completely away from the spacer. place the mouthpiece between your teeth and seal your lips tightly around it, press the inhaler once and breathe in slowly and deeply. hold your breath for 10 seconds or as long as you are comfortable and breathe out slowly.

repeat steps 3 to 10 after 30 seconds, if anotherdose is required.

best inhaler

best inhaler

how to relieve your sinus infection in 20seconds do you have a tongue and a thumb? if you do,you already have everything you need to clear your sinuses in less than 20 seconds! a stuffy nose often occurs as a symptom ofanother health problem such as a sinus infection or the common cold. usually, these healthproblems are minor i.e. allergies, nasal polyps, chemical exposures, environmental irritantsand hay fever. when the lining in the sinus cavities getsinflamed due to irritants, bacteria or viruses, your nasal passage swells and gets blockedup, making it hard for you to breathe. nasal congestion usually clears up withina week, but with this natural remedy, you

may not wait that long to breathe easy everagain! how to clear your sinuses in 20 seconds ready to breathe easy? follow these simplesteps: push your tongue against the top of your mouthand place your thumb between your eyebrows. apply pressure with your thumb for 20 seconds.your sinuses will begin to drain. how does it work? you might be wondering how a little pressureon a bone can lead to a drain of sinuses. it has a scientific reason behind the technique.according to lisa destefano, d.o., an assistant professor at the michigan state universitycollege of osteopathic medicine, this technique

causes the "vomer" bone to rock back and forth.the back and forth motion loosens congestion, allowing your sinuses to drain. if the technique mentioned above doesnã­twork for you, donã­t rush to your drug store for a solution just yet! try these four naturalhome remedies. you may already have these ingredients at home. 1. organic apple cider vinegar mix eight ounces of warm water with two tablespoonsof apple cider vinegar and one tablespoon of honey, or take one tablespoon of applecider vinegar three times daily. you sinuses should clear up in a few days.

you could also mix half a cup of apple cidervinegar with half a cup of water, heat it on the stove, and inhale the steam with yourmouth and eyes closed. 2. turmeric turmeric contains curcumin, which contributesto this spiceã­s anti-inflammatory properties. sprinkling some turmeric on your next mealcan help to treat the nasal inflammation that his blocking up your sinuses. 3. nasal saline rinse this is not the most comfortable solution,but many people rely on a saline rinse to clear up their sinuses. the mixture can consistof a quarter teaspoon of sea salt/pickling

salt with one cup of warm water. this rinsegets poured through one nostril and out the other to clear the sinuses. if you have never done a saline rinse before,ask someone for assistance and read and follow the instructions on the package very carefully. 4. oregano oil oregano oil isnã­t as widely available oras cheap as the above natural remedies, but if you happen to get your hands on this oil,simply ingest it, or steam it over the stove and inhale it to effectively clear up yoursinuses. this oil is an effective sinus infection treatment.

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best inhaler for asthma

best inhaler for asthma

natural asthma inhalers: asthma mist - http://natural-asthma-inhaler.com/

Kamis, 27 April 2017

best inhaler for allergic asthma

best inhaler for allergic asthma

asthma is a problem in the lungs in whichthe lungs produce excess mucus, causing a feeling of constriction in the lungs, notallowing the person to be able to breathe properly or take deep, full breaths. thereare two types of asthma: extrinsic and intrinsic. one is caused by the body’s own immune systemproducing excess mucus and lung constriction; the other is a problem when a person breathesin cold air, breathes in a chemical agent, or exercises too much, causing restrictionwithin the lungs. conventional medicine treatments of asthma are typically steroidal or non-steroidalmedications in inhaler form. they can be used on a daily basis to suppress symptoms or onlyas needed. long-term use of steroids can cause muscle weakness, adrenal suppression, weightgain, and fluid retention. asthma typically

begins early in childhood. some of the causativefactors include genetics; secondhand smoke exposure during childhood; exposure to environmentalmolds, allergens, or pollutants; food sensitivities; multiple antibiotic prescriptions before theage of one; and multiple vaccines. to diagnose a patient with asthma, i first do a medicalintake of their recent symptoms. i then listen to their lungs for any abnormal sounds thatindicate they are having an asthmatic attack of some sort. i also perform a blood testto assess for food sensitivities that may be irritating their condition, and i may performa stool test to make sure that they're digesting their food properly. asthma is a conditionin which the body’s immune system inappropriately responds to the environment, so my goal withtreatment is to control the body’s inappropriate

response by introducing anti-inflammatorynutrients and removing dietary irritants. dietary irritants include diary, wheat, gluten-containingfoods, soy, eggs, white potatoes, nightshades, red meat, and caffeinated products. so insteadof eating these foods, i ask my patients to instead eat organic green vegetables, fruits,and whole grains. i also prescribe vitamin c and fish oil for their anti-inflammatoryproperties, magnesium to help relax smooth muscle in the bronchial airways, probioticsto support a healthy digestive system, which in turn helps support healthy immune system.for patients with ongoing asthma attacks, i’ll prescribe a botanical formula thatcan remove excess mucus secretion, open up the airways, and control the asthma attack.in fact, these botanicals are so powerful,

they can eliminate the need for an inhaler.asthma is difficult to treat; however, when patients follow my protocol, they have a decreasednumber of asthma attacks, decreased severity of those attacks, and rarely do they needtheir inhaler.

best inhaled steroid for asthma

best inhaled steroid for asthma

adult asthma patients will soon have a newtreatment available to them. i'm shelby cullinan your latest health news. the us fda approved breo ellipta, which isan inhaled corticosteroid, to treat asthma. the once-daily asthma treatment from glaxosmithkline,or gsk, and theravance inc. is only approved for use in adults. the fda approved breo elliptaafter the drug was studied in more than 12,000 patients in 23 trials and appeared safe andeffective. according to gsk, breo ellipta may raise patients' risk of certain hearteffects, such as increased pulse, raised blood pressure and irregular heartbeat. speak toyou doctor about the best treatment option for you.

best inhaled corticosteroid

best inhaled corticosteroid

respiratory distress in children is causedby either upper or lower airway diseases. upper airway obstruction is recognized bythe presence of stridor, a high pitch sound often audible without a stethoscope, mainlyon inspiration but can also be heard on expiration. aspiration of a foreign body, especially frequentin the 1-3 age group, must be ruled out. a history of aspiration may be offered by thepatient or family. remember to get imaging – while the foreign body may be lucent,look for signs of hyperinflation. another serious cause of upper airway obstructionis viral laryngotracheobronchitis or croup. patients with croup have a stridor and usuallyhave a cough that sounds like a seal barking. a dose of systemic corticosteroid will alleviatethe obstruction for the course of the illness,

but nebulized epinephrine may sometimes benecessary to reduce the edema quickly to relieve the acute respiratory distress. a rare butsevere complication of croup is bacterial tracheitis. lower airway obstruction presents with shortnessof breath, a prolonged expiratory phase, wheezing and accessory muscle use. in children over two years old, viral inducedasthma is the most common cause for this presentation. inhaled bronchodilators are used for symptomaticrelief, but corticosteroids are essential to settle the lower airway inflammation.bronchiolitis is caused by a viral infection in infants less than 12 months of age andwhile it may present very similarly to asthma,

it does not respond to bronchodilators orcorticosteroids. recommended management include supportive care such as intravenous hydration(if the infant is too distressed to feed) oxygen supplementation (if the oxygen saturationis below 90%) and ventilatory support (for impending respiratory failure).pediatric pneumonia often presents after symptoms of viral upper respiratory infections, butwith fast breathing and lung crackles. lung radiography confirms the diagnosis and thepattern of infiltrate or consolidation may guide antibiotic selection.

best drug for asthma

best drug for asthma

how to treat asthma with ginger! asthma is a commonly known lung disease. thisdisease causes mild to severe difficulty in breathing and this again entirely dependsupon if it’s an acute asthma or a chronic one. the difficulty in breathing is causeddue to blockage in the airways of the lungs and this is also considered as the initialmost sign of asthma. there is no definite cause or reason for asthmabut there are many things that could trigger asthma attacks such as: pollution.dust. psychological factors such as stress, depressionand despair.

hereditary.excessive smoking. being a passive smoker.kids with respiratory infection. sudden changes in the weather.food allergies. childhood infections.allergy to certain medications. the factors that can trigger asthma attacksare many and one of the most common one is dust and pollutants. these not just triggerasthma attack but can also be the primary cause for asthma. as far as the treatment is concerned for asthmathere are many over the counter drugs available in the market but often these medicationscan be quite addictive.

so the next best way to answer the query abouthow to treat asthma is with the help of some easy and natural home remedies. these remediesare made using completely natural ingredients and this makes them safe, side effect freeand very affordable. they have also been proven to give guaranteed results in curing and preventingthe body from asthma attacks. this is exactly what we shall be discussingabout in this article today. in this article we have listed out some of the most popularand highly recommended natural asthma remedies using ginger. from the use of many other natural ingredientsto treat asthma one of the most commonly and highly effective natural ingredient is ginger.

ginger is a root vegetable which is knownto heal and treat the symptoms of asthma naturally. it has also been proven be many scientificresearches that the consumption of ginger during asthma attack also helps in easingout the breathing process and reduces the breathlessness. this is also the main reason why most of thehome remedies to cure asthma mainly promote the usage of ginger in them! so here are out top most recommended and trendingsolutions for your query about how to treat asthma with ginger. treat asthma with ginger using home remedies!!!

1. ginger & salt remedy: ginger is known to be a great natural sourceof anti inflammatory and anti viral properties. this makes it one of the best natural ingredientsto get rid of the symptoms of asthma. try this remedy and get an instant relieffrom the breathlessness caused due to asthma! ingredients: small ginger pieces ( 2 to 3 ).salt ( 1 pinch ). small bowl. directions: 1. take a piece of ginger and cut it intobite sized small pieces of about 2-3.

2. now add into a small bowl and sprinklesome salt over the ginger pieces. 3. mix it well so that the ginger is wellcoated with salt. 4. now consume this as and when you get anasthma attack as it immediately helps in clearing out the airways in the lungs and allows youto breathe easily. 5. this is one of the most instant naturalremedies for asthma. 6. one needs to consume this remedy only whenyou get an asthma attack. 2. ground ginger remedy: this remedy is for the ones looking for naturalcures for asthma and don’t have that much free time on hand to sit and prepare a homeremedy for the same.

it’s a quick and quite effective one andone can easily follow this one everyday just before going to bed. ginger soaked in water helps in doubling upthe potency of ginger to cure the symptoms of asthma and also prevents the chest andnasal congestion. ground ginger ( 1 tsp ).water ( 1 ⽠cup ). small mixing bowl. 1. take a small mixing bowl and into thisadd in the water and the ground ginger. 2. now mix this well until the ground gingeris well dissolved in the water. 3. now take a tablespoon of this mixture justbefore going to bed.

4. if you feel uneasy after consuming thisthen you can also drink a glass of warm water after consuming this.5. follow this routine if you are worried about how to treat asthma with ginger at home.6. continue doing this everyday for at least 2-3 weeks or until you don’t experienceany symptoms of asthma.

best asthma treatment

best asthma treatment

when he was a baby, he was really, reallysick. he had gone to preschool and had an incidentwith peanut butter, and that's when we first realized that he had a peanut allergy. we went to another clinic here in little rock,and they began treating him and giving him testing, and they told me at the time thathe was too young for allergy shots. so, we began the long process of finding theright medications that were perfect for him. and, his medication list got very lengthy. because we were not happy at the other clinic,and, i feel like that it was the best move that we could have made for him.

and, we've been very pleased with the outcomethat he's had. the seasonal allergies have been somethingthat we have struggled with ever since he was a baby. it's difficult as a working parent havingto be home with him all of the time because of the allergies he's developed. and the seasonal allergies, especially inthe springtime. the puffy eyes, the wheezing. when we started at little rock allergy, hewas tested for those seasonal allergies. i saw an immediate positive response fromcarson when he began allergy injections.

they do have a lab. and, they can make our own extract, and that'sa big benefit for us, because that does not have to be submitted off to another companyand take a chance on the extracts being made, and not being made correctly. don't just treat the symptoms. don't go to the store and just get the zyrtecand try to self medicate. and don't get on the websites and try anddiagnose your own kid. the problems are still going to be there,even though you've treated the symptoms. big, big improvement.

i've been really pleased with the directionthat the doctors here have taken with his care, and the way the allergy injections havetaken care of carson. he's able to play sports and be more involvedin some of the things he loves to do.

Rabu, 26 April 2017

best asthma remedies

best asthma remedies

hey, guys, dr. axe here, founder of draxe.comand doctor of functional medicine. in this video, i'm going to share with you the topherbs and supplements and diet to naturally treat asthma. if you've ever struggled withasthma, you know that it can be really a debilitating condition. it can really affect your lifein many different ways. people can really sort of live in fear of having that asthmaattack. but i will tell you this, that there are some things you can do that can reallyhelp eliminate asthma by about 99%, if you follow the steps that i lay out for you inthis video. the first thing you want to do if you haveasthma is take a good look at your diet and eliminate foods that cause food sensitivitiesand foods that really cause your body to produce

more phlegm. so food sensitivities, the mostcommon ones include things like wheat products or grains. any type of grain, for the mostpart, especially gluten-containing grains, those can cause food sensitivities. dairyproducts, especially because of a1 casein, found in a lot of conventional dairy, thatcan cause food sensitivities. also things like soy and corn and peanuts, those can causefood sensitivities. you may even go and get a testing done toget an igg and an ige antibody test done, to see what foods you're reacting to. it'ssomething that most doctors can do, especially a doctor of functional medicine. you can gosee them, and they can lay out this test for you. or in fact, you can even look up iggtest online on google, and you can actually

find a test and take it at home and get yourresults back in a couple of days. so number one, know your food sensitivities. number two, eliminate foods that cause phlegmbuildup, especially sugar, excess sugar consumption, along with dairy, and then even things likebananas. those things are phlegm producing. eliminate those from your diet. now, the diet that you want to follow to helpeliminate any type of phlegm and help reduce asthma symptoms is going to be a diet that'sgoing to be high in vegetables, fruits, easily digestible protein, and omega-3 fatty acids.so vegetables and fruits, the reason they're beneficial, they're not going to cause youto produce phlegm. also, they're high in enzymes

and phytonutrients, which help eliminate phlegmand really open up your airways, and they reduce inflammation. especially, citrus fruitsare great. pineapple is great. but again, loading up on the vegetables and fruits shouldbe the core of your diet. the next thing would be think warm foods likebone broth soup. those warming foods help open up your capillaries. they are very easyto digest. so a big bone broth soup is an ideal meal for somebody. bone broth soup isgreat because bone broth contains amino acids of proline and glycine, and glycine reallyhelps support the liver, also supports the lungs, helps open up those airways. so again,if you've ever heard chicken soup is good for the soul or chicken soup is good whenyou're sick, the reason being is when you're

sick, think about it, you've got congestedsinuses, bronchitis, and congested chest, and bone broth helps open up those airways.so a bone broth soup on a regular basis should also be at the core of your diet. and last, but not least, omega-3 fatty-acid-richfoods, chia seeds, flax seeds, grass-fed beef, wild-caught fish, getting more omega-3 reducesinflammation and can definitely help asthma. now, the top supplements you want to consider,if you really want to support your body in healing asthma, are going to be quercetinis one of the best. quercetin is found in citrus fruits, so adding in oranges and grapefruitand lemon and those sort of fruits into your diet, a great place to start with asthma typically.

also, the supplement bromelain, bromelainactually does come from the core of a pineapple, so consuming some pineapple, you're goingto get some bromelain. or you can take a bromelain supplement. there's also a supplement combination that'spowerful, effective at treating asthma, and that's a combo of n-acetyl-l-cysteine andvitamin c. n-acetyl-l-cysteine, or nac, is the precursor to glutathione, and glutathioneis an antioxidant that really helps support respiration and detoxification of your lungs.so n-acetyl-l-cysteine, typically about 500 milligrams, with vitamin c, that combinationof nac with vitamin c is a powerful combination at actually helping heal asthma.

and then last thing i want to mention herewith asthma is also taking essential oils that can support the airways. if you are havingasthma issues, sometimes taking a mixture of peppermint oil and eucalyptus oil can bebeneficial. but you always want to test it on your body first because for most people,it helps open up their lungs, but i know sometimes people with asthma, they tend to react todifferent things. and that's a similar thing with the citrus fruit. i mentioned that quercetinis amazing, typically, for people with asthma, but again, if you're sensitive to something,you obviously do not want to use that if you have asthma. but again, if you can follow those tips, iguarantee you're going to see great results

in relieving your asthma. if you want to learnmore about natural asthma treatments, cures, and remedies, make sure to check out the dr.axe website. just search asthma. that's draxe.com. also, hey, make sure you subscribe here toour youtube page. i've got a lot more videos coming out on natural cures using food asmedicine. hey, guys, this has been dr. axe. thanks for watching.

best asthma preventer

best asthma preventer

three-quarters of homes that were builtbefore 1978 have lead paint in there so lead paintwas banned because we found out hey it's killing usseems like a very good reason to ban something so exposure to lead causes permanentbrain damage and half a million american childrenhave elevated levels on the lead in theirblood why because they're living in these houses that have the lead paintlead poisoning is linked to lower iq's learning disabilities and get this evencriminal behavior

in fact there is up benchmark study thatwas crazy it came out i wanna say about a year ago probablylittle less than that that show the connection between lead poisoning and crime so when the gasoline was lighted there there was a spike in the crime lee rate wherever the areas that had themost leaded gasoline now of course there's a causation correlation problem there butthey look into it further

and they found out that even forindividuals yeah the lead is actually i'd seems to be willing to aggression andviolence and crime amazing amazing said you were never thought that right so %uh twenty years ago congresscommitted to addressing the problem byestablishing what's called the office of healthyhomes & lead hazard control so since then the office has partneredwith states cities and the private sector

to remove the lead from over 200,000homes obviously a step in the right directionand a noble thing right well they're still a lot of leadto be removed but the sequester cut the alreadyunderfunded program by six million dollars now this obviously cripple their ability tohelp but wait a second it gets worse so therepublicans now have a brilliant idea they proposed to cut it even more findadditional $64 million dollars so now

children are gonna get sick from leadpoisoning and are you ready for the park that makes iteven worse now i know you're probably thinking of how can it possibly get worse they cut additionthey got another the proposing to cut it even more and wealready know it means to all these horrible problems how could possibly getworse are you ready according to a 2009 studyquote for every dollar spent on controllinglead hazards seventeen dollars to 221 dollars wouldbe returned in health benefits

increased iq higher lifetime earnings tax revenue reduce spending on social onspecial education and reduced criminal activity so using the most conservative estimate i love seventeen dollars in benefits for everydollar invested the six million dollars that sequestration already caught fromletter removal programs what cost our country at least 100 and two million dollars your first the house republicans cart of $64million

that would cost over one billion dollars so my question is what happened deficit hawks i thoughtthe republicans care deeply about balancing the budget and the deficit what you care about that then you shouldfund the program to remove the lead you idiots the science is clear on this and by the way that shouldn't even comeinto consideration really because you should care deeply about the healthconcerns which is a bigger problem so i give you

your any it corrupt government at work

best asthma medicine

best asthma medicine

sanjay, what are the treatment options for asthma? when i discuss treatment options for asthma with my patients the first thing that i talk about is that there are this group of medicines which are the ‘rescue medications’, versus the ones that are ‘controller medications’. so the rescue means that they should be used only when you need rescue in terms of improving your shortness of breath. and controller means medications that are used on a regular basis irrespective of how you feel and which are controlling the asthma and preventing asthma attacks in those patients.

the rescue medications, actually there’s one major category which is the use of what we call ‘short-acting bronchodilators’. now, bronchodilators are medications that relax the airway muscles, and the short acting ones means that they only act for a short period of time. that's the classic rescue medication. albuterol is the one that we use most commonly. then controller medications fall into two groups: one is the long-acting bronchodilators. so, it’s again bronchodilators that relax the muscle but they last for a much longer time,

so you need to use them only once or twice a day. they are not meant for rescue use, they only meant to be used on a regular basis as you take a pill on a regular basis for a condition. and then the other very important group of controller medications is what we call inhaled corticosteroids. the inhaled corticosteroids are the ones that deal with the inflammation and swelling, and those are kind of central to the treatment of asthma. the downside is they don't give any immediate benefit,

but i think it's a very important that i spend a fair amount of time with my patient saying that this is the medication that's actually dealing with the fundamental problem or cause of your asthma, the swelling or inflammation in the airways. so, do you adopt a similar approach? i do absolutely. and i think it's an important thing for everyone to recognize, as you said, a rescue versus a controller because a rescue medication is a medication

that makes you feel good right then and there. so it's very easy to say that that seems to be the best medicine for your asthma. but it's important to recognize that it's not treating that underlying inflammation, swelling and using it too much can actually cause your body to become a little bit resistant to it as well, where it might not work as well in the future if you overuse it. so if you have what we call persistent asthma, where your asthma is active enough that the physician thinks a controller is needed, it's really important to use that on a regular basis even when you're feeling well.

steroids are the biggest category of controllers and we know they're very very effective for most of the cases of asthma. and there are other options. there are medications which come in a form of pills. one of them is a group of medications known as leukotriene antagonists. they also attack the inflammation in asthma, but they are not as effective or as broad as the inhaled steroids are. and then of course you know in very difficult cases we get in to biological drugs which deal with the antibodies

that are causing the inflammation or the allergic inflammation in asthma. but those are in really in more severe patients that we reserve those medications. i think the most patients with asthma would end up being treated with a combination of rescue plus controller medications in most situations.

best asthma medication

best asthma medication

in an asthma attack, the muscles of the airpassages in the lungs go into spasm. this makes the airways narrower, making itdifficult to breathe. this can be triggered by an allergy, a cold,or smoke. at other times, someone may have a suddenattack with no obvious trigger. if you think someone is having an asthma attack,there are five things you may see: they may have difficulty breathing orspeaking they may be wheezingthey may be coughing a lot they may be distressed and anxiousthey may have a grey-blue tinge to the lips, their earlobes or their nailbeds.

people with asthma usually know how to deal with their own attacks by using their reliever inhaler usually with a blue cap- at the first sign of an attack. but if they don’t, or if the attack is severe,you may need to help. when treating someone having an asthma attack,keep calm, reassure them and advise them to use their reliever inhaler straight away. advise them to use a spacer if they have one. ask them to breathe slowly and deeply to helpthem control their breathing. sit them down in a comfortable position. if it doesn’t get better within a few minutes,it may be a severe attack.

get them to take one or two puffs of theirinhaler every two minutes, until they’ve had 10 puffs. if this is their first attack, the attackis severe, they are not getting better, they are getting worse or they are becoming exhausted,call 999/112 for emergency help. help them to continue to use their inhaleras needed. keep checking their breathing, pulse and levelof response. if they do become unresponsive at any time,treat a casualty who is unresponsive. so remember, reassure them. help them to use their reliever inhaler.

if the attack is severe call 999/112 for emergencyhelp and monitor their level of response. if they become unresponsive treat as an unresponsivecasualty. and that’s how we help someone with an asthma attack. if this video has been helpful to you, helpsupport st john ambulance by going to sja.org.uk/donate.

best asthma inhaler

best asthma inhaler

natural asthma inhalers: asthma mist - http://natural-asthma-inhaler.com/

Selasa, 25 April 2017

best asthma inhaler brands

best asthma inhaler brands

albuterol is a prescription medication usedto treat bronchospasm (narrowing of airways) and to prevent exercise-induced bronchospasm.albuterol is in a class of medications called bronchodilators. it works by relaxing andopening air passages to the lungs to make breathing easier. albuterol comes as a regularrelease tablet, an extended release tablet, and a syrup to take by mouth. albuterol mostcommonly comes in a solution to be inhaled either with a nebulizer or inhaler. this medicationmay be taken once every 4 to 6 hours to prevent asthma or as a rescue medication during anasthma attack. common side effects include fast heartbeat, shakiness, and nervousness.for more information on this medication and all other medications, explore the rxwikiencyclopedia on the web or on your mobile


beconase inhaler asthma

beconase inhaler asthma

what does cromolyn mean? cromolyn. noun 1. (pharmacology) ; a chemical substance, acting as a mast cell stabilizer.

azmacort inhaler

azmacort inhaler

take the cap from the mouthpiece. shake the autohaler well. hold upright and push the lever up until it clicks into place. breathout completely away from the inhaler. keep the autohaler in your mouth. place the autohaler in your mouth & breath in slowly and deeply. you'll hear a click when the medication is released. keep breathing in until you take a full breath. remove the mouthpiece and hold your breath for 10 seconds as long as you are comfortable and breath out through your mouth or nose . press the lever down. repeat 2 to 7 steps after 30 seconds, if another dose is required. replace the cap.



fifteen year old chris is having a severeasthma attack. his immune system has made what could be a fatal mistake ("i can't breathe") and is shutting down his airways. ("i really can't breathe") without help from the medical team, chris' body may shut down completely ("i'm going to die").the breathing tubes in chris' chest are squeezing tightly shut, and filling with sticky mucus,blocking his vital oxygen supply. if he is not treated soon, he will die. here's a reallylife-threatening episode of asthma. asthma is pretty common in our community, and mostof the time it's not this life-threatening, but this one is quite serious. chris' allergicreaction has tricked his immune system into shutting down his airways, blocking vitaloxygen to the rest of his body. the drugs are supposed to help the muscles around chris'airways to relax, but there is a problem.

the mucus stops the drugs from reaching his blood supply. time is running out - chris' body takes emergency action. his shoulders and neck muscles swinginto action to help inflate his lungs, but even this is not working. as the pressuremounts, the team must find a treatment to get the drugs past the mucus. chris is byno means an isolated case. one in nine australian children suffer from asthma, but for christhe situation is looking dangerous. chris is currently having ventolin or salbutamolthrough a nebuliser which is breathing into his lungs. this acts on the muscles aroundthe small airways and helps to open them up. unfortunately sometimes when the airways arevery closed down, the salbutamol doesn't reach the areas that it needs to get to. if the inhaledventolin is not working, then we often will go

to a different form of medication - againa relaxant for the muscles around the small airways, and it helps to open those airwaysup, and it's given as a one-off dose over about 10-15 minutes in severe asthma. inside chris' body, theairways start to open as the drugs take effect. air finally returns to chris' lungs, inflatingthe three hundred million tiny airsacs. at last, he can breathe. chris seems to be feelinga lot better now. the intravenous medication seem to have taken effect. he still is verytired, because he's been working very hard with his breathing, but we're a lot happierwith his clinical progress now. chris was admitted to intensive care for three days,with a further three days in a medical ward before being sent home. he is now back atschool, playing soccer, and is aware that

it is important to look after his asthma andtell his teachers and family when he's not well. chris had always expected other peopleto look after his asthma, but after this emergency, he now understands that he must recognisewhen he is having asthma and follow his asthma action plan. before leaving hospital, chrislearned what asthma is, how to manage his triggers, what his medications do, and howto use them correctly. chris now uses a spacer to have his medication. he also learnt howto recognise when his asthma was worse, and the need to follow his asthma action plan.chris has taken control of his asthma.

asthma without inhaler

asthma without inhaler

if you want to know how to stop wheezing,watch this video complete. "wheezing" refers to a high-pitched whistlingsound produced while exhaling or inhaling. to stop wheezing, you'll need to clear yourairways and make it easier for your lungs to process each breath you take. depending on the underlying cause, professionalmedical intervention might also be necessary. clear the air. keep your living environment clean to stopwheezing. removing irritants from the air you breathecan stop wheezing and associated difficulties caused by external sources, so you shouldkeep the air in both your living and working

environment as clean as possible. dust, sweep, and vacuum your home and officeregularly. if you have pets, you may need to vacuum everyother day to adequately control pet dander and fur. clean or change the filters in your heatingand cooling system. use hypoallergenic filters to trap more respiratoryirritants. run a small air purifier in the rooms youspend the most time in, including your office and bedroom. don't smoke and don't share your space withthose who do.

you should also avoid traveling in industrialareas with heavily polluted air. wear scarves during cold weather to stop wheezing. cold air can actually cause your lungs andairways to tense, which may cause or worsen wheezing. if the temperature is cold enough for youto see your breath, you should wrap a scarf around your nose and mouth before steppingoutside. the scarf should warm the air before it reachesyour airways. additionally, the scarf can serve as an extrafilter to ward away airborne respiratory viruses commonly spread during the cold winter months.

avoid potential allergens and other triggersto stop wheezing. exposing yourself to food allergens and environmentalallergens can cause wheezing, and foods that produce mucus can make wheezing worse. avoid as many of these triggers as possible. foods that produce mucus include dairy products,bananas, and sugar. if you have difficulty identifying your allergens,you may need your doctor to perform an allergy test. treat seasonal allergies that cannot be avoidedwith over-the-counter antihistamines. severe seasonal allergies might need prescriptionmedication.

inhale steam to stop wheezing. take a steamy shower or run a vaporizer inthe room you're currently sitting in. as you breathe in the steam, the warmth canrelax tense airways and the moisture can thin the mucus clogging them. to the same effect, try boiling 1 quart (1l) of water mixed with 8 to 10 drops of peppermint oil. once the water begins to evaporate, take itinto a small, closed room and breathe in the steam. don't hold your face directly in the steam,however, since doing so could cause burns.

stay away from potent smells to stop wheezing. strong odors aren't necessarily bad for youwhen your lungs are healthy, but if your airways are stressed, they may cause those airwaysto restrict further. this can both cause and worsen wheezing. chemical odors, like paint and chemical cleaners,can be some of the biggest culprits, but you should also avoid things like perfumes andheavily scented soaps or shampoo. change your diet. stay hydrated. drink more water than usual when your wheezingstarts.

instead of aiming for eight 8-oz (250-ml)glasses per day, try to drink 10 to 12 glasses. drinking water can make mucus thin and loose,making it less likely to clog your airways and cause wheezing. other hydrating fluids, like herbal tea andcitrus juice, can also help, but you should avoid fluids that can dehydrate you (alcoholand caffeine) and those that may produce more mucus (dairy milk). drink something warm. warm fluids hydrate the body while soothingstressed airways, so they can relieve and even end many wheezing episodes when theystart.

herbal teas are some of your best options. try sipping on ginger tea, chamomile tea,or licorice root tea. adding 1 tbsp (15 ml) of honey to your teacan also soothe stressed, raw airways while acting as a mild antiseptic agent. hot soup is another good choice, especiallyif you stick with broth-based soups. creamy soups may not help quite as much sincethe dairy they contain can thicken and produce more mucus. take fish oil capsules to stop wheezing. some studies suggest that omega-3 fatty acidscan strengthen your lungs.

while this may not result in an immediateend to your wheezing, it can help stop wheezing in the long-run. fish oil capsules are a great way to supplementyour diet with omega-3 fatty acid, but you can also increase your intake naturally byconsuming fish like salmon, mackerel, and sardines. try something spicy. if you've ever eaten something spicy whensuffering from head congestion, you probably already know that spicy food can cut throughthat congestion quickly. similarly, eating foods that contain cayennepepper can help wheezing, as well.

cayenne pepper causes the fluids of your bodyto become active, thereby pushing more fluids through your body and causing mucus to thinout. as the mucus thins, it should become easierto breathe. diagnose the underlying condition. wheezing is only a symptom of some other condition. you should schedule an appointment with yourdoctor to determine the cause of your wheezing if the symptom lasts for more than a few days. thanks for watching video. we hope our video was very helpful to knowhow to stop wheezing.

don’t forget to like this video and subscribeour channel for further health updates.

Senin, 24 April 2017

asthma treatment

asthma treatment

the other point used for treating asthma iscalled cv22, and it's located in this area. if you find the mid-line of the front of bodyand go upward, you will find an indentation here, and in this depression, this is thepoint we call the ten-to. we use that to treat acute asthma attack. if we apply the cortisoneintravenously, we cannot stop an asthma attack for a couple of hours and the patient is indanger. then in china, we usually use this point. we first insert needles to penetratepoint two inches, and then we change the direction of the needles downward and against the sternumfold and go point back one inch, and this can instantly stop asthma. also, we usuallyuse that to treat problems of the throat and also difficulty to swallow things.

asthma treatment without steroids

asthma treatment without steroids

my name is tom kalm. i'm at the asthma andbreathing institute in albuquerque, new mexico. i've been receiving treatment; i think i'vehad four treatments of acupuncture and i've been using herbs to make tea, and i've beenfollowing the prescribed consumption of the tea appropriately. i've noticed that my asthma,my inflammation in my lungs and my bronchial passageways is substantially decreased. rightnow i'm not on advair, nor proventil, the two medicines that i take, and i can breathe,and i can breathe fine. i worked all weekend physically on memorial day. i believe thatthe treatment, even though i'm only approximately 1/3 of the way through it, has been an effectivemodality of treatment and increased my lung capacity. i do want to say that we have measuredmy lung capacity. it has increased. my blood

oxygen level increased with the first treatmentfrom 92% to 97%. i felt, while i was getting the treatment myself become alert. i feltlike my mental acuity was enhanced and increased. i believe that to be because of the increasedoxygen level and a number of other things: including better circulation. i recommendthe treatment it is effective and i can tell you that two months of my prescriptions, evenpurchasing them at costco pharmacy, the steroids are more than the entire first series of treatmentwith chinese herbs and acupuncture. with this treatment i believe that my baseline is goingto moved to a place where i don't have to worry about having asthma medicine or steroidsor a rescue inhaler with me. i will be able to be a like a normal person without asthma.that the problem with steroids. when you run

out, if you are some place where you can'tget your prescription refilled and you have asthma, and you have an acute episode, youhave a real problem. so this treatment is an economic bargain. it gives me a safetymargin. because i don't have to carry anything with me. thank you.

asthma treatment without inhaler

asthma treatment without inhaler

natural asthma inhalers: asthma mist - http://natural-asthma-inhaler.com/

asthma treatment steroids

asthma treatment steroids

in terms of treating asthma, there is a newprocedure called bronchial thermoplasty, which has been approved by the fda for treatingpatients with severe, persistent asthma. they’re patients who are calling the office, they’re on and off prednisone,they're in the emergency rooms, they're missing school, they're missing work, they're hospitalized;those are the patients we can treat with this procedure called bronchial thermoplasty. theprocedure is actually three separate procedures. we treat the bottom of the right lung first.about a month later, we treat the bottom of the left lung, and then a month later, thetop of the both lungs. it’s an outpatient procedure. we perform the procedure in thebronchoscope suite. a patient would come in, they would have a hospital gown put on, andan iv put in. we work with our anesthesiologists.

they're completely asleep for the procedure.the procedure lasts for about forty-five minutes. the way the procedure works is that we delivershort bursts of thermal energy to the airways. physiologically, that thins out the smoothmuscle. when a patient breathes in an allergen, they’re less likely to be broncospastic,because of the decrease in smooth muscle. the vast majority of patients can go homeafter the procedure. there is concern that the procedure will cause an asthma flare.to mitigate that or minimize that, we pretreat patients with prednisone. eighty percent ofthe patients have a significant improvement following treatment. there's less hospitalizations.there's less trips to the emergency room. there's less prednisone use. there's lessasthma flares. we now have data that suggests

that the effects last for at least five years.i've had patients who feel better after the first treatment. most people feel better afterthe first or second production--so one to two months after the treatment. the biggestproblem with bronchial thermoplasty is getting insurance pre-approval. its a relatively newprocedure. in order to combat that, at pulmonary associates, we have personnel dedicated towork on the pre-approval process. asthma is a major problem in the lehigh valley. notonly do we have very high levels of allergens, but we don't have the best air quality andtogether those two factors, make it difficult for people with asthma and other respiratoryconditions. this technique is really special. not only is it helping patients manage theirasthma, but its really helping them manage

their lives. the problem with asthma is that,you never know when the next flare is coming. one day you can be good and the next day,you're not and what we found is this procedure gives patients control back in their lives.

asthma treatment side effects

asthma treatment side effects

natural asthma inhalers: asthma mist - http://natural-asthma-inhaler.com/

Jumat, 21 April 2017

asthma treatment inhaler

asthma treatment inhaler

>> all: how to use an inhaler! >> iggy: hi emily! are you ready to show ushow use an inhaler? >> coltron: inhalers can come in all differentshapes and sizes. >> broncho: now how are you supposed to useit? like this?? >> iggy, coltron, broncho: noooo!!! >> iggy: that’s right, emily! you can’tjust puff it in your mouth! the medicine will get stuck in your mouth and throat, and itneeds to get all the way to your lungs! what do we need, emily? >> broncho: perfect, emily! you have a spacer!

a spacer is a tool to make sure you get theright amount of medicine from your inhaler and that it goes to your lungs! >> coltron: spacers can also come in all differentshapes and sizes. >> iggy: now, emily is going to show us theright way to use and inhaler with a spacer! first, sit up and take the caps off of yourinhaler and spacer. >> coltron: when you’re ready to use it,shake the inhaler for 5 seconds, and put it into the open end of the spacer. >> iggy: then, tilt your head back a littleand breathe out as much as you can then, put the mouthpiece of the spacer inyour mouth.

make sure you seal your lips around it tight! >> broncho: now press the inhaler to puffonce and breath in slowly and deeply for 3 to 5 seconds. >> all: 1, 2, 3, 4, 5! >> coltron: then hold your breath for 10 seconds,or as long as you can! >> all: 1, 2, 3, 4, 5, 6, 7, 8, 9, 10 >> iggy: now take the spacer from your mouthand blow out slowly. if you have trouble taking that one big deepbreath, you can take 3 or 4 slow deep breaths instead.

if your doctor wants you to take two puffs,do it all again on more time! >> broncho: yaaahoo, you did it! good job,emily! thanks for helping us today! >> iggy: see you later, emily! >> all: bye, emily!

asthma symptoms

asthma symptoms

we were married 64 years, and we'd both doit over again. i wouldn't trade it for anything. you better not. when you get to be a certain age and you can'twork anymore, you have to try to get used to living on a limited budget, plus you don'thave that cash flow that you had before. it made it difficult to get financing, to dothe things we needed to do in our down-sized home. our house needed insulation. it hadoriginal windows in it, so it needed duel windows. we found out our duct work was leaking25%. that of course, wasn't good for our asthma. once we met mark the hero representative,we were able to finance this. our average bill was 450 bucks a month. now it's like, 210. i can't believe the difference. i save more than i pay.

a lot of people say, "at your age, why wereyou going to spend that kind of money?" i said, "i might live for another 10 or 15 years.why not?" why not live comfortably? our asthma symptoms have improved, because i've been able to sleep all through the night without having a coughing spasm. hero is just a real hero to me, because they've helped me do something that i couldn't do.

asthma steroids

asthma steroids

>> the controllermedicines are steroids. when parents hear that theirchildren will be on steroids every day, they're concernedabout several things. >> steroids--at firstthey did concern me. because, i guess, as anatural reaction you hear steroids and it definitely--it alarms you. >> the steroids that we useare natural products of your adrenal glands. they're a normal part ofthe chemicals that your

body produces. >> the most important concernsseem to be about growth. >> however, there's a numberof studies now that show that children with asthma who useinhaled steroids for many, many years developand achieve the full growth potential that they wouldhave achieved had they not gotten inhaled steroids. >> many people are concernedthat taking medicines for their asthma will make themdependent on those medicines

or that, if they use themregularly or every day, that they maynot work as well. >> but this reallyisn't the case. there are a number ofstudies that show that asthma medicines work betterif you take them every day, and they don't lose theireffectiveness over time. >> i've seen my childvery, very sick, and i realize that heneeds these medications. and it's just like anyother type of illness.

if you have medicationthat can help your child, you have to givethe medication. >> families need toknow the facts about controller medicines. these medicines are safeand work through natural ways that the body healsswelling and inflammation. they use low doses delivereddirectly to the airways where asthma occurs. controller medicines havebeen shown to prevent flares

and emergency visits andreduce symptoms for children with asthma. in order to work best,controller medicines must be taken every day. children receivingcontroller medicines do need to see a doctor regularly tomake sure the dose and type of controller medicineare right for the child.

asthma steroids side effects

asthma steroids side effects

this is what happens when you eat garlic onan empty stomach! garlic is mainly preferred as a part of manydelicious dishes as it adds to the taste, whereas many people avoid intake of garlicdue to its strong smell. apart from the taste and smell there are manymedicinal properties of garlic, which make it active ingredients of the alternative medicine. empty stomach intake of garlic- is it good? yes, it is good to eat garlic on an emptystomach. there are many studies which have supportedthat garlic act as a natural antibiotic when consumed on an empty stomach.

it is recommended to eat garlic just beforethe breakfast to keep the bacteria on the bay. some of the prime benefits of eating garlicon an empty stomach include: hypertension relief– it reduces the stresslevel and provides relief from hypertension. prevents heart problems– due to effectivefor blood circulation garlic is good for the heart and prevents many heart troubles. improved digestion– garlic provides relieffrom stomach problems such as diarrhea and promotes proper functioning of bladder andliver. it is also effective to stimulate the appetiteand digestion.

with all these benefits, garlic is well knownas a healing food since ancient times. use of garlic in alternative medicine: the alternative medicine has highlighted theimportance of garlic to cure many diseases. it is mentioned that garlic helps in detoxificationof the body and thus keep up safe from infections. it is used to get rid of worms and parasitesas well as to prevent diseases like diabetes, typhus, some types of cancer and depression. one should keep a note that people who areallergic to garlic should avoid the raw intake as it can lead to skin issues, headache aswell as an increase in body temperature. if you see any of such symptoms after intakeof garlic, then stop the consumption immediately.

it is also suggested that people on hiv/aidsmedication should avoid the intake of garlic as it can lead to side effects. if you don’t like the strong smell of garlicthen you can use the pill of garlic as a natural supplement to take advantage of the benefitsof garlic. other benefits of garlic: garlic has many more benefits and is activelyused to cure many diseases. here is in detail how you can use garlic tocure some chronic diseases at home. for respiratory diseases- you can treat manyrespiratory diseases like lung congestion, bronchitis, asthma as well as tuberculosisand pneumonia.

garlic treatment for tuberculosis: it is a very simple process to cure tuberculosiswith the help of garlic treatment. 1. take a bulb of a garlic and divide it intovarious portions. 2. you can directly consume the raw garlic oradd it in the sauce along with the egg yolk and oil. 3. if you don’t like the taste of raw garlicthen roast it to light brown color in the

oven. 4. consume the entire bulb of garlic every dayto cure tuberculosis. garlic treatment for bronchial disease: you can make a special infusion at home usinggarlic to cure bronchial disease. take 200gm of garlic,700 gm of sugar and 1000gmof water. now, boil the water and add garlic to it. let the garlic boil for 2-3 minutes and thenadd sugar to the mixture. heat the mixture for another 2 minutes andthen keep it aside.

5. drink 3 tbsp of this solution daily to curethe bronchial disease. garlic treatment for chronic bronchitis: to cure chronic bronchitis, the garlic homeremedy is the excellent solution. see how to prepare the garlic infusion totreat chronic bronchitis. take 40 gm of garlic, wash it properly andcut down into small pieces now, add 100gm of 90 proof alcohol and storethe mixture in the airtight bottle. let the garlic soak in the alcohol for 5-6days. later strain the liquid and drink 1 cup ofthe solution every day to cure chronic bronchitis.

in order to treat asthma and catarrhs youjust have to drink warm water with 15-30 drops of garlic extract every day. you can breathe the vapors of garlic by infusionof garlic in boiling water to treat constipation and hemorrhoids. the application of garlic provides quick relieffrom earaches. another important application of garlic isto treat colds and fight warts. you just have to apply a few drops of garlicextract on the affected area to cure the problem. keep in mind: there are numerous properties of garlic andhealth benefits which make it preferable if

you add it in your daily diet. the medicinal properties of garlic will protectyou from various infections and internal diseases which in turn help you to remain healthy.

asthma steroids names

asthma steroids names

>> welcome to the wednesday afternoon lecture. today we have dan littman who will talk about very intereting interaction between the microbiome and the immune system. he is an investigator at the howard hughes medical institute

and coordinator of the molecular pathogenesis program and kimmel professor of molecular immunology at the skirball institute at nyu. dan got his undergraduate at princeton and got m.d. ph.d. in molecular biology at wasu. following that did a post

doctoral time with richard axel at columbia, then set up his own inventory at ucsf while where for the next ten years he was assistant professor associate professor and full professor. but since 1995, he's been at the nyu school of medicine where he is both investigator of hhmi but

also kimmel professor. he's been recognized by a number of honors, notably election to the national academy of sciences in 2003 and the ross prize, and the coly prize. his investigations he's going to tell you about understand ways in which t lymphocytes acquire

functional properties during development in the thymus and how this is influenced busyingnals initiated by distinct commensal microbes in the intestin. so here we are at a time when one would be tempted to say and would say correctly, that there

is a revolution going on in our understanding of the microbiome and ability to assess what's happening particularly in the gi track but there also seems to be period of rapid advances in immunology an putting to two together is an example how sometimes the most exciting

science happens at those interfaces between disciplines and there could be nobody better to represent that this afternoon in this space than dan littman. please join me in welcoming dr. dan littman. [applause] >> thank you so much, francis.

it's really a great honor to be invited here. thank you so much for having me. i have a lot of very warm feelings for the nih for many reasons. i was here in 1976 just as i was starting my ph.d. work as part of my m.d. ph.d. because

advisers were finishing their post-doctoral fellowships here and they were in transition to st. louis and i helped them with the move after spending the bicentennial summer in washington which was a very special time. so as francis mentioned, i will

tell you about our work on trying to deconvolute how microbiota interacts with the immune system. and in particular with t lymphocytes. the title that i have here, i'm not exactly certainly we think the microbiota act as in

instructing t lymphocytes as to their fate. but also in deciding whether when they're on their way to one fate or another which branch they're going to talk. there's a lot of plasticity in the immune system and i will tell you a little bit about the

various options. we have heard of course a great deal about the microbiota during the past five to ten years. we now know the commensals within us contribute to insulin resistance or sensitivity, they have a very important role in obesity.

there's beautiful work in jeff gordon's group, a pioneer in this area showing that their microbiota that in twins who are discordant in terms of weight pre-dispose mice to the same phenotype as the human host. there are also examples of the microbiota influencing the

central nervous system and behavior. i will tell you a little more about this towards the end of my talk and the microbiota have been implicated in the from here, from the carrie laboratory has shown commensal microbes influence responses to cancer

therapy both chemotherapy and immunotherapy. we have a poor understanding what's going on there but we think some of the work we and others are doing to try to understand the responses of the immune system may contribute to eventually getting an

understanding there of how these microbes might be manipulated in treatment of cancer. our entry into this field molecule called r 1 gamma t, a transcription factor that is a nuclear receptor similar to glucocorticoid or estrogen receptors.

it has ligands of the -- in the cholesterol family, in the cholesterol biosynthetic pathway though the precise ligand is not identified. we think there are multiple ligands. this is a molecule we discovered years ago as being involved in

the thymus for survival of immature thymocites that give rise to cd4 and cd8 cells in the periphery. at the time we started working on this, we also found that it has a role in lymphoid organ development in development of patches and lymph nodes, but the

real excitement in this field came subsequently when it was found that our r gamma t has a role in certain classes of t-cells and in a lymphoid cells type 3 lymphoid cells. i will tell you a bit about each of these different cells, not so much about gamma delta t-cells.

what i will focus on is th 17 cells because it was really discovery of cells by several groups most prominently dan kua that set us on the way as i will tell you about briefly here. so when we first started working on r 1 gamma t and realized role in inductions of lymphoid organs

we found that it's expressed in a cell that was first described by (indiscernible) that eventually was named lymphoid tissue and user cell. this is found in the fetus for development of lymph nodes and secondary lymphoid organs but also found postnatally in

tertiary lymphoid organs such as a structure that occurs in intestine under the epithelial layer, this is called a crypto patch. what this consists of are these r gamma t positive innate lymphoid cells and it's surrounded by dendritic cells

and it's senses the state of microbiota across the single cell epithelium and upon signaling recruits b lymphocytes to become an isolated lymphoid follicle. and gerard, a post-doc in the lab made a knock in of gfp in the r 1 locust in homozygous

knock in mice which gene product is null, there are no structures frm bud in heterozygous mouse we can follow expression of gfp in cells of normal copy. (indiscernible) a new post-doc in the lab we missed earlier, that is that they're not just these bright gfp positive cells

that are innate lymphoid cells that don't have any other kinds of hematopoi ting markers for lineages but there is intermediate gfp populations here that are t-cells that express the alpha beta t-cell receptor, around the same time i received a call from dan who

told me they were look at these mysterious cells that were responsive to interleukin 23. in collaboration with (indiscernible) in dan cord's lab we began look at the cells and quibblingly were able to show -- quickly were able to show in this gfp intermediate

cells there were expression of intracellular interleukin 17 in the gfp r gamma t negative t-cells. there was no negative expression of il 17. this was the way we got into this field these were most abundant in intestine.

so it's been known since the mid 1980s about th 1 and 2 cells, i don't need to tell this adience about this. the late bill paul was a pioneer in this area, one of the heroes in the area of t-cell biology and bill's laboratory did a great deal on characterizing the

molecular features of these cells. the th 1 cells are dependent on the transcription factor d bit and they make interferon gamma, generally required to kill intracellular pathogens but also implicated in autoimmune disease and the th 2 cells are dependent

on transcription gamma factor 3, il 4, 5 and 13, very important for controlling infection with paracytic worms but they also contribute to allergy and asthma through production of cytokines. these were the cells though to be major types of helper cells until the mid 2000s, then with

the advent of discovery of cells that make il 17 they are dependent on gamma t it's clear these cells make other cytokines including into interleukin the 2. these are cells required to control extra cellular microbes i wrote pathogens, but not only

pathogens but also commensal microbes including both bacteria and fungi. the cells are very important repair of tissues at barrier services. primarily epithelial services and they are also implicated in autoimmune inflammatory disease,

there's enormous attention paid to these cells. and i will tell you a bit later about the various cytokines that are required for the generation of these cells. a fourth type of cd4 positive t-cell is regulatory t-cell. t reg cells differentiate,

develop in the thymus, thymic natural t regulars but also peripheral induced tregs that express fox p 3, dependent on transcription and all these cells are really essential for restraining these other types of t-cells and preventing autoimmune disease.

and as i will show you, the induced treg in intestin also express r 1 gamma t. the th 17 cells are ones that have really been at the center of studies of auto-immunity during the last half dozen years or so. and i told you about their

importance barrier surfaces and controlling infection with these pathogens here. but these cells have been implicated in these different kinds of inflammatory diseases. i should say psoriasis is the best validated because antibodies against interleukin

17 and interleukin 23 are tremendously effective in therapy for psoriasis. however that targets il 17 may not only by th 17 but also very likely by gamma delta t-cells. some of these other diseases also appear to be th 17 related. a lot of oar thread dees

arthropathies are dependent on th 17 >> rheumatoid arthritis has a th 17 component, inflammatory bowel disease search and seizure dependent on th 17 cells within some of the other cells that make interleukin 17. probably steroid resistant

asthma as well as ms have th 17 components. i put here as my question mark autism spectrum disorder, i will tell you about a model in mice. in which certainly in that model th 17 cells appear to have a role. so this is just an example of

what we are able to show as soon as we understood th 17 cells were most abundant in the intestin in the lamina propria. they're positive in the -- in terms of microbiota present there but when animals were treated with antibiotic or derived germ free there were

essentially no il-17 producing cells in the intestin of these mice. so this is work again of yvonne and he made observation that took us to study it is microbiota. he found the same strain of mice obtained from different sources

differed in the proportion of th 17 cells among cd4 cells in the intestine. so mice from jack's laboratory had few cells, 1 or 2% cd4 cells whereas mice from -- typically had 15% cells making interleukin 17a. what he was able to show was

help with collaborator kenya handa in japan, this was simply due to a difference in one single bacteria species and that is due to the presence of segmented fill mentos bacteria in mice from this source. this is a gram positive spore forming an aerobic bacteria,

different from taxons of bacteria described but probably it's related to the clostridia. these bacteria you can see in these films that cover the villi in the ilium. and they're completely absent in mows mice obtained from jackson laboratory.

you can see that in a transmission em here, these form segments and they embed themselves in the epithelium of the i willial in the ilium and cause a active polymerization action, we understand nothing about molecular mechanism involved here.

we're able to obtain fecal material from animals that were monoassociated with sfb and gavage germ free mice here they have no production of il 22 or il 17 in their cd4 cells and within a week of gavaging you see massive inductions of these cytokines this helps protect

mucosal barrier from pathogenic bacteria but at the same time make animals susceptible to developing arthritis in a mouse model we study in combination with diane and kristen, this is an example of the protection from ad hearing effacing bacterium there's considerably

less adhesion and there's also less weight loss in these animals colonized with citrobacter. on the other hand, the flip side is that in the kb by n mouse model of arthritis which diane and chris to have had shown no disease when animals were

derived germ free, colonization with sfb alone within only a few days now leads to thickening of the jointses and to inflammation and arthritis. and this is work of joyce wu in collaboration with evo yvonne in our lab. and what joyce was able to show

is that though this disease is dependent on antibody response and and body against a self-protein, it requires th 17 cell polarization. this is what sfb is achieving here. so this led us to consider that there maybe something similar in

humans with rheumatoid arthritis z to what have been observed in this animal model. jose sheer at the time was a rheumatology fellow at nyu, now on the faculty. and jose decided to look at introduced to the mouse gi track in the colon led to inductions

of regulatory t-cells and as i will show you many of these regulatory t-cells are specific for the microbial antigen elicited. these. so just to show you that work, actually this is work by mo shu who is a post-doc in our lack

and mo compared inductions of t-cells by segmented fill mentos bacterium and helicobacter. i told you about induces th 17 response under what we consider homeostatic conditions. there's no sign of inflammation in these animal, th 17 cells are abundant and do not promote

colitis. these are found typically in the ilium in the terminal ilium. sfb control nonnization. helicobacter hepatocuss is in the colon and it can induce a pathogenic type of t-cells response in models of colitis. so fiona has pioneered this

field and shown introduction of naive t-cells into animals that lack any t or b cells in rag knockout mice threads to colitis that is dependent on mixed th 17 th 1 response that cells making il 17 and interferon gamma. we want to see what is the t-cell response under

in her case this kind of colitis require there be colonization with bacteria, most often helicobacter hepatocuss, if one blocks il 10 production in helicobacter there's a similar inflammatory colitis. so what mo decided to do was to isolate t-cells from the

intestin of mice, colonized with helicobacter and identified the t criminal receptors of -- on these cells where elicited by helicobacter and make t-cell receptor transgenic mice as well as generated mhc tetramers to be able to track these particular which turned out to be specific

for heel doe backtor -- helicobacter antigen. he used a combination of t-cells specific for sfb and t-cell specific for helicobacter in animals that were colonized with both of these bacteria. so using eye toe type to distinguish between t-cells

specific for either bacterial antigens, i show you comparison between these here, because now when he recovers t-cells from the lamina propria in the mice you see the cells specific for sfb become r 1 gamma t positive cells, test are th 17 cells non-pathogenic.

helicobacter specific t-cells by and large become fox p 3 cells, shown here, which also express ro1 gamma t. this is the hallmark of these types of t-cells that differentiate in the intestin to become regulatory t-cells shown to have unique properties

different from other t-cells, the t-cells that do not express fox p 3 express chemokine receptors an transcription factor bcl of and these are follicular helper cells involved in the production of antibodies. so what happens when these are introduced, these cells are

introduced into il-10 knockout mice? i told you that in il 10 knockout mice, combination leads to colitis. what we see is these cells now differentiate into ro1 gamma t positive cells for the most part.

unlike the cell specific for sfb these cells are pathogenic. i will explain to you what that means. in a moment. now repopulated with these two types of t-cells, you see helicobacter specifc t-cells express not only il 17 on the x axis but also interferon gamma

on the y axis so this is one of the hallmarks of the pathogenic t-cells on the other hand the sfb specific t-cells in the il 10 knock out only express interleukin 17a and no interferon gamma. and when we have done rna sequencing to compare these

populations, also single cell rna seq we see there's hardsly any difference in the presence or absence of il-10 of these whereas helicobacter specific cells changed dramatically in properties after exposure to the il 10 deficient background. so this takes me to the topic of

pathogenic th 17 cells in these mouse models and whether there maybe such cells in human. there may be such cells in human and there have been called th 1 star cells by frederick salusto who first described them. these cells in the mouse are dependent on the interleukin 23

receptor. i told you that early on dan kua showed il 23 signaling leads to up regulation of interleukin 17 in vitro and it's required for pathogenesis in various mouse models of auto-immunity. so in particular there was an experiment done by a group in

london showing that using fake mapping that many of the cells that initially had expressed interleukin 17a went later to express interferon gamma and that process was dependent on interleukin 23 receptor. and only in the presence of interleukin 23 receptor could

these cells be pathogenic in a model in auto-immunity model of experimental autoimmune encephalomyelitis. we think something similar maybe occurring in human. because fredericka described cells that express chemokine receptors, ccr 6 which is a th

17 related receptor as well as cxcr 3, a th 1 chemokine receptor downstream of transcription factor tbet. these double expressing cells also produce interferon gamma, these are cells she called th 1 star. and joe casino via at

rockefeller found patient families that had immunodeficiencies with deficiency in ro1 gamma t they're known for ro1 gamma t, these cells were lacking and the individuals still had classical th 1 cells making interferon gamma in response to viral

infections. and both fredericka and john also found that these are cells that are particularly responsive to microbacteria. if these individuals from these families lacking ro1 gamma p were inoculated with bcg, they developed disseminated infection

and couple did not survive because the star cells are required for controlling these -- this type of bacterium. the microbacteria. what is special then about these inflammatory pathogenic th 17 cells? lynn w uk has taken a different

approach to look at these, that is to use a rag knockout mice which he reconstitutes bone marrow from il 23 receptor sufficient and receptor deficient mice and then subjects these animals to a couple of auto-immunity models as well as colonization with sfb.

the auto-immunity models are to look at central nervous system infiltrates, i told you about and sfb colonization i told you about. he did single cell rna sequencing in collaboration with -- who is at nyu and genome center.

looking initially at cd4 positive t-cells from the central nervous system in mice in which there was inductions he was able to cluster cells in to different categories shown here. cells had fox p 3 and interleukin 10, il 17 a, interferon gamma and gmcsf,

these are properties what have been defined described as when he looked at distribution of receptor sufficient deficient cells were under-represented in this pathogenic population here. but il 23 independent cells enriched here a regulatory type population we don't think

contributes to the disease. what happens then upon colonization with sfb? if we now look in the intestin at cd4 cells what we see is that there are regulatory t-cells that express fox p 3, cells here, which fall into the category of those that make ro1

gamma t and thymic derived and there what might be consider to be more classical conventional th 1 type cells that make interferon gamma over but there are no cells that make both interferon gamma and il you have instead these what we consider homeostatic th 17 cells

down in this category over here. so we're obviously very interested in trying to understand what regulates the cells going one direction or another. vijay has done beautiful work in this area in which he has identified several candidates

that maybe involved in this process. we're still trying to understand what the relationship is between induced regulatory t-cells and th 17 cells. and we would like to know, we know il 23 is required for these we think they differiate h from

what might be a homeostatic th 17 cells, we know that il 10 restrains this differentiation, and we don't know exactly where these treg cells come from though we think they likely polarize from naive cd4 positive we also know that these cells are absolutely required to

restrain this process of expansion of pathogenic th 17 we have data which if we completely eliminate these transcription factor in these cells, we're able to see the cells and see spontaneous so coming back then to what might be occurring upon

colonization, with sfb there's inductions we see inductions occurring first in the mesoteric lymph node within three days and a few pho days later these are found in the lamb ma propria where they are making interleukin a and f and il 22. we see cells distributing

broadly throughout the other parts of the intestine to distal lymph nodes and also to spleen. that may explain t-cells elicited here in the gut mucosa by microbiota may contribute in some ways to auto-immunity. that's been the goal to understand what it is that

trigger auto-immunity that colonized with certain bacteria. to do this we started taking a closer look at this inductions of ro1 gamma t and il 17a. during time colonization with sfb. i told you already that sfb is mostly in the terminal ilium.

we don't see any at all. we see a change in gene expression quicker -- and the genes highly epiregulated are the ma'am amyloid proteins 1 and 2, i will tell you about that in the next part of this talk duodenum and colon shown here he saw similar proportions of ro1

gamma t positive cd4 t-cells we don't have to stimulate the cells e vivo, we can take them directly out of the the lamina propria and look at gfp expression. we wanted to know what is it about the ilium that's special that allows inductions of

effector functions here. and he performed a series of genetic experiments and also antibody blocking experimentment one shown here we focused on the amyloid a proteins. we're able to use the t-cell receptor transgenic t-cells that are specific for sfb and

introduce them into mice that either were not colonized with sfb or were colonized with sfb. the cells were labeled within the intracellular cfc for proliferation. if we look in the mess tearic lymph node there's no inductions of cell proliferation in the

absence of sfb but with sfb there's good proliferation shown in animals recipients that lack the amyloid a protein genes there's still proliferation. maybe a little retarded but quite good proliferation. there's inductions of ro1 gamma t in the meds tearic lymph node

if we look in the illinois yum lamb ma propria, we see something different. look at il 17 a inductions you can see that in these t-cell receptor transgenic cells many cells make il 17a but few comparatively few of the cells make il 17a in the absence of

sero amyloid a. -- serum amyloid arc. this is due to a role of the microbiota, in this case particularly sfb activating the type 3 innate lymphoid cells to make interleukin 22. earlier randy longman in our laboratory found that

mononuclear figcytes or monocyte derived cells that make interleukin 1, 23 and tnf family member tnf sf 15 or tl 1a through production of these cytokine, able investigate the lymphoid cells to produce il 22 and il 22 acts to protect barrier.

miriam's lab at the same time found csf 2 or gmcsf also made by ilc 3 in response to microbiota contributes to homeostay at this and ex-- homeostasis and expansion of regulatory t-cells in the lamina appropriate preia. what they found is there was

inductions of il 22, upon if they lack interleukin 23 receptor, in this case the receptor primarily on innate lymphoid cells you can see upon colonization with sfb, there's less inductions of saa 1 and 2 in the epithelium of these mice. and this is looking in a log

scale at the rna level. this and others led us to the model that i show here. sfb colonization there's a local short circuit in which the monocyte derived cells making interleukin 23 act on receptor innate typhoid cells that acts on receptor in the intestine on

the -- in the epithelium, activating phospho3 and that leads the expression of saa 1 and 2 within the first few days of colonization. at the same time monocyte derived dendritic cells traffic to the draining lymph node, polarize t-cells through

mechanisms we don't understand yet, to become ro1 gamma t positive. these are distributed throughout and outside the intestin but here locally where we have serum amyloid a protein there's enduction of the il 17 of the effector cytokine.

let's propose a step 2 model in the differentiation and activation of th 17 cells versus specification in a draining lymph node and can be monitored by ro is gamma t expression. and inductions of effector function that in this case on serum amyloid a proteins to a

large extent. p p p p p i wouldn't say completely dependent, we say an example of endogenous adjuvant that might have a unique or special role on th 17 cells, this led us to endogenous adjuvants may change threshold for activation of

self-reactive t-cells that might be induced by sfb. that may lead to pre-disposed animals to autoimmune disease. that is a hypothesis we're following. so we focused because of these results on serum amyloid a known for many years in the clinic

because they are acute phase reactant, much like c reactive protein. these are lipoproteins associated with high density protein, and retina in the palacena. they're produced in liver for acute responses to infection.

enormous increases in circulating levels. they are also elevated in tumors in synovium of rheumatoid arthritis patient and in the serum in autoimmune disease and it's been reported in multiple sclerosis patients for example. it's a highly conserved family

of genes and there have been multiple reported receptors although it's unclear which might be physiologically important, toll like receptor 2, the formal peptide receptor 2 and cd 36 have been reported as receptor, so far we haven't found a function for any of

these in what i'm going to show you now. so jim young lee started looking at the role of saa which we found works directly on t with recombinant saa 1 and 3 he is able to see a really substantial increase in the proportion of cells that express

interleukin 17a even just in the presence of interleukin 6. interleukin 6 and tgf beta are cytokines that induce th 17 cells from naive cd4 positive t-cells and john o'shey's group here has looked at other conditions for looking at tgf beta independent differentiation

of cells with il 6 il 1 beta and il 23. you can see in these differentiation conditions, adding in recombinant saa 1 leads to major increase in the proportion of il 17 producing and what's really interesting is that if we now look at ro1 gamma

t expression here we see that even without any difference in ro1 gamma t expression in these cases, we see a big increase in il 17a, consistent with the idea of this is a second hit second signal that activates the effector function of the cell. so june decided to look in

models of auto-immunity to ask whether saa might be important and you look at saa knockout mice gotten from fred debeer in kentucky but introduced by crisper a mutation in the third saa gene saa 3 expressed by macrophages in the lamb ma propria upon colonization with

so he compared in the immunization model the wild type saa triple income out mice and what e h sees is -- triple knockout mice and he sees attenuation of disease in acute phase shown here but also chronic phase of disease here. i won't show you the data but we

know that this attenuation seem to be mostly a function of the absence of saa 1 and 2. whereas this more rapid recovery here, seems to be mostly function of saa 3. we're beginning to try to understand what might be going on there.

so you can see that after immunization with mog and adjuvant there's rapid increase in circulating saa 1 and 2, this is in the knock outs here for sa 1 and 2. and this is due to expression from the liver because you can see both saa 1 and saa 2 are

highly up regulated upon immunization primarily in the liver but there's nothing no activation of saa 3 in that organ. on the other hand looking at the central nervous system you see no effect of saa 1 and 2 but there is inductions of saa 3,

this turns out to be made by microglia and by monocyte derived cells that invade the central nervous system after immunization. so what june also noted was when he looked many the chronic phase of disease he saw animals had various levels of disease scores

but also varied in their circulating saa 1 and 2. he was able then to compare the level of saa 1 and 2 in the circulation to the disease score and he saw a remarkably strong correlation here the higher the circulating level of saas the greater the disease.

consistent with the saas having a role in the disease then he looked at another model of eae that was developed in vijay's lab using t-cell receptor transgenic mice which t-cell receptor is specific for a peptide of the myelin protein of mog.

so these 2d 2 cells are differentiated in vitro, polarized to become inflammatory th 17 cells with this combination of il 6 and tgf beta and subsequently interleukin 23. when introduced into wild type mice, that leads now to paralytic disease, to the eae.

he wanted to compare now to saa 1, 2, 3, knockout mice, i only show results with saa 3, there's a mild defect upon introduction into saa 1, 2, double knock out but you can see introduction into saa 3 knock out almost completely protects animals from the disease as shown by percent

of animals with disease and the average disease score. what's also interesting is gating on raw gamma t positive cells in animals sufficient or deficient for saa 3, you can see that even though there are gamma t positive cells in the knockout mice that go to cns many are 17a

consistent with the idea there might be a second signal coming from saa to facilitate production of effector cytokine in this microenvironment. so to put this two step model in context of pathogenesis, what we think then is that saa 1 and 2 in sfb specific t-cells

contributes to the cells locally becoming positive for interlocking 17a and f. on the other hand in the pathogenesis model of eae in the cns we see a role for saa 3 in the expression of the pathogenic cytokines and the ability of these cells to induce disease.

we think that i showed you example with sfb of these cells going to the lamb ma propria where they can be subject to this induction by saa, we think that similarly these cells make their way to the central nervous system but maybe by circuitous route.

we don't know whether they are derived from these cells first induced in the intestine, in this case potentially in the small intestine but i will show you in the eae model we think it's they are induced by saa produced by the liver. another important question here

is do the th 17 cells that go to central nervous system need to be cross reactive with th 17 inducing bacterial antigens. is there some kind of molecular mimicry involved in the autoimmune disease, i will be happy to discuss this after my lecture but our inclination is

to think that's not the case. we do think the microbiota are critical in this particular model of auto-immunity in the mog induced inducedeae as shownhere. we treat with ampicillin or advantage co-mycin. we protect them from the paralytic disease.

you can see the neomycin do not have this kind of an effect. so it's giving us the opportunity now to begin to look to see which bacterium are involved here, this is in mice that lack any sfb. this is not an sfb dependent effect.

to put into context we think the micriobiota do in fact program the cells to become ro1 gamma t positive in this polarization. thereafter immunization with mog in presence of adjuvant there's production of systemic sae 1 and 2, these proteins act on primed th 17 cells, activating them,

maturing them. they express now chemokine receptor crr 6 that allows to traffic to the central nervous once they get there, we think that they can cause local inflammation and positive feedback process activate production of saa 3 by the

myeloid cells there and now the saa 3 acts to generate the -- to induce the pathogenic cytokines and that leads them to chronic inflammatory disease. so these are all testable hypotheses now to try to understand how these cells make their way from being just prime

cells to being actually p pathogenic t-cells. so what i was telling you we think there's a two step model of the prime cells and effecter cells that can be generated by a variety of different means. and these could be homeostatic or pathogenic.

and contribute to autoimmune disease, e we think potentially harnessed for pro or antitumor affects. i will show you another example this two step model is important. that is a model for autism called the maternal immune

activation model. so this particular model was developed affidavit there were reports based on population studies that women who had had infections late in first trimester of pregnancy were more likely to have children with autism spectrum disorder.

the model developed was to either introduce a virus or later just polyic which activates toll like receptor 3 into pregnant mothers day 12 and a half of gestation. that leads to behavioral abnormalities in offspring persisting into adult life and

as well as to morphological abnormalities developing in the central nervous system. this is a model that was championed by the late paul patterson, caltech. and about a decade ago paul published a paper showing that this mia phenotype in the

offspring requires mother be specific for interleukin 6. this paper in journal of neuroscience. at that time a fabulous post-doc in my lab, june hu, joined the lab, he was a graduate student at caltech who knew paul patterson's work.

we were beginning to work on th 17 cells, this was now more than ten years ago. and we knew il 6 is involved in inductions of ro1 gamma t and th 17 cells so we propose this would be involved in this animal model, through inductions of th 17 cells.

so we got a pilot grant from simon foundation for autism research and began to look at this. there's three cardinal symptoms of autism, social interaction defect, communication defects and stereotypic or repetitive behavior, all can be modeled in

animal models in mice debatable whether they are related to what's going on in human. it is what we have available to work with. what june initially did was to reproduce paul patterson's result showing inductions of il 6 shortly after polyic injection

but he also showed inductions of interleukin 17a and in fact the interleukin 17a in circulation stays all elevated for longer than il 6 does. we can block with antibody against il 17. and importantly we have made a conditional knock out mouse for

ro1 gamma t which we could knock it out specifically in t-cells using the cd4 cre to cross to and you can see that after polyic in these mice there's no elevation of interleukin 17a in the mother. he was then able to use this as a tool as well as antibody

against il 17 to see what might occur. one of the first things he showed by doing in situ hybridization was that there is expression of interleukin 17 receptor a in the outer layers of the cortex in the fetus embryonic day 14 and a half, you

can see it here. you can see that after polyic there's actually an increase in experience here. it is known that il 17 receptor is regulated in the positive feedback matter by its own signal, il 17 binding. then we're able the start doing

behavioral assays in wild type and mutant mice in the offspring of wild type and mutant mice. this is the marble bearing assay, a repetitive behavior assay in which the mouse is asked to bury marbles in its bedding and there's a tremendous increase in this kind of

repetitive behavior after polyic treatment of the mother. we eliminate this in the model is lacking ro1 gamma t in her specifically t-cells. similarly one can look at social interaction assay, interacting with another animal here under this cup here, or inanimate

object here, a normal mouse spends twice as much with another mouse and with the inanimate object. and what we see here is after polyic, this is basically a 50/50 ratio, we basically restore preference for the social interacting mouse in the

-- if the mother is lacking ro gamma t in her t-cells. and there's also a nor foe logical defect that we observe that's quite severe that you see here in the cortex, sustaining with various markers for cells in developing cortex in the fetus day 18 1/2 six days after

injection of polyic, blocking il 17 in the mother basically abrogates this abnormality. finally, june with his wife gloria chow a neuroscientist together did injections across the uterus into ventricles of the fetuses and injecting il 17a or pbs or interleukin 6.

only after il 17a injection behavioral defects as well as morphological defects. and in this case we looked at behavioral defects of communication defect though we also saw other behavioral defects i told you about. you can see the morphological

defect as well here. and the last thing i wanted to tell you about is that this is requires microbiota specific microbiota in the mother. that's why i want to link the parts of my talk here. when june was recently able to do it, june has his own

laboratory now at u mass and wooser, he's looking at mice with or without sfb or mice colonized with a mix of bacteria from kenya honda, human bacteria from human that induced th 17 cells in mice. and was able to colonize a mothers and look at il 17

inductions and behavioral defects. you can see here after introduction of the human bacterium in this case and polyic there's a tremendous increase in il 17 production without increase in the introduction of human bacteria,

just black 6 flora from jackson laboratory, there's little il 17a induced by polyic. this corresponds to the behavioral phenotypes i told you about, the localization index, marble bearing, anxiety assay and interaction assay, social interaction assay.

what we can conclude is that in this model the microbiota are absolutely critical in the mother for the priming. and following that priming, of ro gamma t positive cells a second signal inducedded by polyic allows production of il 17 which crosses placental

barrier through mechanisms we don't understand and acts only ic receptor in the central nervous system, the fetus must have intact il 17 receptor in order for the phenotype to be manifested. and that leads both to the developmental phenotype, the

cortico phenotype as well as behavioral abnormalities. so this has interesting implications for humans. we don't really know whether there's anything like this in human, there's no question autism is caused in most of the cases by genetic influence but

there is a known environmental influence. some of that environmental influence could be due to the question here in maternal infection, activation in a subset of women, those women with a particular kind of microbiome that renders their th

17 cells more active larger numbers of ro gamma positive t-cells this is not something we can answer easily but i hope that this study is going to set the stage for doing more investigation in this area. i will stop there. this is june hu, the latest work

was done by san du kim, post-doc in his lab. all the work on the neurophysiology as well as histology in the cns was done by gloria chow at mit. we did much of our early behavioral work at nyu with chuck hull fer now at the

university of colorado collaborated with ken honda and cohhi in terms of microbiota and san woning kim made the conditional knockout mice for these are some of the folks that i mentioned as i went along. betty yang back in china, he was a south carolina for a while.

and he identified the specificity of the sfb induced wendy woning ucsd did much of the early work on saa inductions and its role on t lymphocytes, we collaborated with raul on single cell rna seq, fred debeer on 1 and 2 mice and kim koje on the microbiota studies.

and i will leave you -- stop there and be glad to take questions. thank you very much. >> the hour is a bit late but we should take questions starting >> great talk. do you think it has direct efects on regulates fox p 3

independent of affects of ro gamma? second part il 10 independent of ability to modulate ro gamma level? >> saa -- we haven't seen effect of saa on upregulation of stacks t 2. >> i was imagining

down-regulation. you're saying you get pathogenic th 17 cells and >> we really don't know if there's a difference how saa influences the homeostatic versus pathogenic. we don't know whether it's a difference between saa 1 and 2

and sae 3 in terms of signaling in the target cells. you could imagine there might be a difference there. we're looking at that now. all those experiments i showed you what we know basically. we can see these affects in vitro that are really dramatic

affects, we haven't looked to see whether saa inhibits regulatory t-cell inductions. we should probably look at that. >> that was fantastic. i wanted to touch on the question of antigenic mimicry, as you know we have some data that points to the fact that

this maybe important. you mention you think that if i understood correctly, saa might be changing the threshold of t-cell activation, through the t-cell receptor perhaps. but then later on in your talk you sort of discounted the possibility of antigenic

mimicry. expand on that. how does that go together? >> we have preliminary data that mog-specific t-cells that i showed you in that model in the knock out model, are still dependent on microbiota. even though they are specific

just for that peptide of mog. so it's very difficult to imagine there's fortuitous cross reactivity of a th 17 cell inducing bacterial antigen with mog. >> from who said the antigen affect built into the microbiota?

and angiogenic effect if such is present have to be on the same book? >> i don't think they need to be on the same. i think they can be separate. yes. and the adjuvant effect can be totally irrelevant to that

model, in the draining lymph node joint lymph node or cns draining lymph node, what have you. but it's still, it's still a hypothesis whether there's a difference in threshold. >> bringing it down to critical realm, with a well known

syndrome toxoplasmosis cmv, herpes, rubella and now zika entering the realm of cerebral abnormalities in terms of hypothesis, in terms of the th 17 in pregnant females in terms of these syndromes have there been any specific studies done? these would be perfect targets.

>> i'm not aware of that. after we got this result i called up tony fauci a year ago when zika was coming to the fore, i thought my god this could be it but obviously that's not the case. zika unfortunately cannot be -- if this was the way zika worked

it would be much more manageable clinically. it would be nice. but that's not how it works. but i'm not aware of anybody having done those kinds of studies with the other infections either. >> thank you.

>> very quickly. >> so considering the large pool and the variations of this regulatory t-cells in the brain versus the intestine, what is it so acute in the autosome? that has an effect other susceptible tissues. you mentioned maternal

local interleukin 17. is it good enough to make such a signature impact on inactivation of the cerebral -- >> you're asking can there be enough il-17 in the s laying in >> no, is there something else, what do you see in autism -- the spectrum, wanting the other

issues with the larger brain volume,is there anything else besides the causing inflammation and causing other affect? >> this is a very limited mouse model. we cannot extend this to human. there is no question il 17 can be sufficient here.

whether in vivo we don't know because when we bombard ventricle with il 17 it may not be actually what happening when fetus is in utero normally getting transplacental il 17. so there could be factors, i agree with that, we don't know that.

we know it's required in the it maybe sufficient. and it is a restrictive model even if it is like some human it will develop a small segment of the spectrum. outstanding work. >> if you would like to continue the conversation and also enjoy

coffee and refreshments please let's adjourn to to medical library but let's thanks professor littman again.