Allergy - Science topic

Allergies in dolphins and cetaceans undoubtedly exist, though little is known about this topic. It may seem like a silly question or joke, but the subject is serious.

Did you know that some corresponding members of the Russian Academy of Sciences have an H-index of less than 5? And, surprisingly or unsurprisingly, they are the children or relatives of leading academicians of the Russian Academy of Sciences.

And for two "health officials", the number of publications with co-authors is off the scale." I wonder if they've read all their publications.

"Having adenoids or tonsils removed in childhood is a fairly common operation, but little is known about the long-term effects. A new study published in JAMA Otolaryngology—Head & Neck Surgery found that removal significantly increased the risk of respiratory, allergic, and infectious diseases later in life, and that the long-term risks of these surgeries deserve some thought by providers and caregivers.

The researchers said that they believe theirs is the first study to estimate long-term disease associations with early-life tonsillectomies and adenoidectomies for a broad range of diseases.1

Adenoids and tonsils are parts of the immune system, helping with pathogen detection and defense. When physicians remove adenoids and tonsils to treat recurrent tonsillitis or middle ear infections, that timing coincides with ages at which the development of the immune system is sensitive, the researchers said.

Previous research into risk has mostly focused on consequences related to perioperative risks and short-term changes in the symptoms treated.

Researchers looked at a population-based cohort study of almost 1.2 million children born in Denmark between 1979 and 1999. The children were included in national registers up to 2009, covering at least the first 10 and up to 30 years of their life. Participants were included if their adenoids or tonsils were removed within the first 9 years of life. Both the case and control groups were selected such that their health did not differ significantly prior to surgery.

A total of up to 1,189,061 children were studied; 48% were female. Of these, 17,460 underwent adenoidectomy, 11,830 tonsillectomy, and 31,377 adenotonsillectomy; 1,157,684 were in the control group.

Adenoidectomy and tonsillectomy were associated with a 2- to 3-fold increase in diseases of the upper respiratory tract (relative risk [RR], 1.99; 95% CI, 1.51-2.63 and RR, 2.72; 95% CI, 1.54-4.80; respectively), including chronic obstructive pulmonary disease.

Smaller increases in risks for infectious and allergic diseases were also seen: Adenotonsillectomy was associated with a 17% increased risk of infectious diseases (RR, 1.17; 95% CI, 1.10-1.25), corresponding to an absolute risk increase of 2.14%, because these diseases are relatively common (12%) in the population.

In contrast, the long-term risks for conditions that these surgeries aim to treat often did not differ significantly and were sometimes lower or higher.

These once-routine surgeries have started to decline recently, as alternative treatments for infections in ear, oral, and nasal cavities have emerged, the researchers said.

Researchers said that although rigorous controls for confounding were used, it is possible these effects could not be fully accounted for.

In an accompanying commentary, Richard M. Rosenfeld, MD, MPH, noted that 2 factors that were not measured, but could have influenced the results, included smoke exposure and antibiotic exposure. Reverse causation also could have been present; for example, children with asthma, allergies, and frequent respiratory infections use more healthcare than controls, are more likely to see specialists, and are more likely to become surgical candidates, he said."

Hi Andrea! I have read some studies about tolerance to allergies over time. These are some of them:

Adaptation to an allergic reaction occurs when the body's immune system recognizes that a certain food protein is not harmful. The immune system forms antibodies and other cells to target and eliminate the food protein, thereby reducing or eliminating the allergic reaction. In addition, some people may develop a type of “tolerant state” meaning they will not experience any adverse reactions or symptoms when consuming the food proteins again.

The exact mechanisms underlying the development of tolerance are still under investigation, though numerous studies suggest that both innate and adaptive immune tolerance may be involved. Innate immune tolerance refers to the body’s ability to recognize components of the food as safe and not initiate an inflammatory response. This requires recognition of the food components as harmless by immune mediators. Adaptive immunity refers to the development of specific antibodies and cells that recognize the food components as harmless and do not initiate an inflammatory response.

References:

1. Chauhan, A., Verma, V., Mohamad, M., & Aggarwal, A. (2017). Immune Tolerance: Understanding the Mechanism. Journal of Immunology Research, 2017, 1–9. https://doi.org/10.1155/2017/5161348

2. Shah, D., & Cole, D. (2016). Tolerance, Allergic Reactions, and Immune Evasion: Insights into the Cellular Mechanism of Tolerance Development. Advances in Immunology, 127, 87–107. https://doi.org/10.1016/bs.ai.2016.05.002

Giorgio Perino

Thank you very much for answering my question in detail.

I'm sorry for the late response.

For a), I am thinking of collecting cells at the very end of the experiment, after sacrificing mice. For b), I use the allergy rhinitis model so it would be better if I could collect cells from the sinuses as well. For c), I hope to mainly collect the inflammatory cells.

About lavage, is it a good way to gain inflammatory cells? Or the epithelial cells be the main cells you can obtain from this method, and the flow cytometer analysis will be difficult?

No, there are essentially 3 major types of immune response to infection: an antiviral response which illicits interferon, a pro inflammatory response that makes il1, il6, tnfalpha etc wich is normally directed against bacterial and fungal infections ( and can lead to cytokine storm) and then the allergic response directed against allergens like ova that generates il4, il10, il13.

In mouse models, balb/c mice are typically used to study allergic responses as thy are inherently more allergic and c57bl/6 are used to study proinflammatory responses and diseases because they are inherently more prone to this type of immune reaction.

Sudeep Kumar Maurya

Thank you very much for the article, I will refer to it!

Yes:Of course!!

La vacuna cubana mambisa fue diseñada para los niños. Le invito a buscar estudios realizados en Cuba al respecto

N. Belloumi it was for post-COVID as well as asthma and COPD patients.

Agreed with dear Arvind Singh

The reason for bleeding in the majority of cases is misdirection of the spray towards the septum, active management in the first instance is stop the spray for a few days and use aseptic or a local lubricating spray. Either lubrication should be applied with the 'non-touch' technique as patients often use their finger or a cotton bud to install the ointment which defeats the purpose.

Prevention is best especially if the intranasal steroids are necessary so I advise the use of the X-Factor approach which is directing the spray laterally towards the medial cants of the eye on the same side thus optimising delivery of the medication to the turbinates and avoiding the septal mucosa as much as possible. This advice which is liked by children was based on a clinical nugget that I received from an experienced German ORL college some year ago which was to present the spray to the right nostril with the left hand and vice versa. This method by crossing fingers for the nose while instructing her led to one of my adolescent patients first suggesting the X-Factor

Interesting - https://www.webmd.com/lung/covid-allergies.

Allergies - a kind of Antigen - Antibody reaction ( Hypersensitivity Reaction ) - Increases the body defence mechanism .

No

Take a look at the following link.

The answer is "Yes". Please see the following RG links.

In adults main cause is DNS or Turbinate pathology

And where are you from ? This is strictly dependent on geographical region and plants that pollinate in your country.

If you type "pollen callendar" + name of your county into the google, you will probably receive a map or any other data you need.

Best,

Lets them to grow and many allergy factors will disappear with age.

Thanks

How looks like the concentration of anti-CCD antibodies in this patient?

تجنب تناول الأطعمة التي تسبب الحساسية

Allergy is a natural reaction from the body to the direction of a particular food, so it is better to move away altogether "to eat food allergens so as to avoid the health problems resulting with my wishes for all health

Unfortunately, I have not this document.

I like the hypothesis as well, but the whole picture is very complicated and poorly understood. The Wikipedia article on the hygiene hypothesis gives a pretty good story about the various related ideas. I think most of us in related fields like and think the hypothesis is at least a partial explanation of the increase in allergies. It may be a part of the increase in a variety of diseases, including some of the autoimmune type diseases. The complete picture is complicated, but bacteria, fungi, protozoans and worms are all a part of the big picture of human health.

Dear Dr. Jenmalm

Interesting articles!

Thank you so much for providing those useful informations.

Best regards,

Naruaki Imoto

Dear Hiroyuki Wakiguchi

Thanks for sharing the information

Regards

Kumanan

When we challenged allergic ships that were sensitive to egg protein, the asthma attacks occurred in two patterns - one immediate, and one delayed like 20 min. later. The only measure we found that was consistent with the clinical findings was the early rise and the late rise of plasma thrombospondin (TSP), which was released from activated platelets. And, the platelet activation was induced by the interleukin and cytokine release. Perhaps you may look at the pattern of the onset of asthma attacks after allergen challenges.

Shih-Wen Huang, MD

This is quite optimistic. The CRISPR system has been reported to make massive deletions in DNA regions other than the target region. Perhaps we have to give it more time.

The Clinical picture seems to be urticaria. May be contact urticaria ( if localized only on the distal arms) or other causes if generalized. In any case firstly treat it by anti-histamine drugs and after almost two weecks of suspension consult an allergist and make the appropriate investigation on ethiology of hives.

I don't think so. The main mediator of prostate enlargement (benign prostatic hyperplasia) is dihydrotestosterone (DHT), a metabolite of testosterone that is formed in the prostate cell by the breakdown of testosterone. The enzyme 5-alpha reductase converts testosterone to DHT.

Please also have a look at these useful links.

The main broblem with IgM is reumatid factor interfearence. Try using RF blocker (commercially available) in the sample diluent

Thank you Dr. Esther Jacob

medication "noncompliance" or "noncompliant" are readily understood in the USA.

Dear Jade Lu Dac,

Please have a look at this PDF attachment.

Good luck!

According to the severity of the case if the patient is severely hypoxic with delirium and impaired conscious save live with intubation followed by epinephrine if condition is hemodynamically stable give epinephrine and wait you may not need intubation

I think philosophy gets a lot of bad press because people both inside and outside of academia don’t understand what philosophy is or confuse it with something else. I’ve also found that many institutions that don’t have philosophy departments or philosophy courses still engage with mainstream academic philosophy under some other guise. Maybe Philosophy would have a larger profile if we renamed it “Conceptual Management and Planning”….

Thank you for your guidance

There is evidence that topical steroids are absorbed systemically. When one eye is treated with topical steroids, the contralateral untreated eye may be affected by the systemically absorbed steroid.

Reference:

Dear dr. Mostafa,

For diagnosis, a detailed history of the lesion and its systemic association is needed. The lesions could be a type of small vessel vasculitis, rash of hypercoagubility state, embolic rashes (given the history of AF) or circulatory insufficiency. These can be differentiated by taking biopsy. But it could be a dermatological dyspigmentation problem, so it is worth to take dermatological consultation as well.

In the US, any of the approved fellowship training programs for allergy, asthma and immunology should be able to help training the staffs who would like to learn the treatment with immunotherapy. If you are not the candidate of fellowship program, you may need to contact with program director to discuss your individual situation.

Shih-Wen Huang, MD

They are handled by Kerafast.  If you check their website, they are available.

IgG4 tends to be rife with false positives. This seems to be due to it commonly representing tolerance to frequently consumed foods vs a true sensitivity. Furthermore, when a positive result overlaps patient symptoms, there tends to be very little correlation with the extent of the IgG4 elevation and the severity of symptoms.

Stapel SO, Asero R, Ballmer-Weber BK, et al. Testing for IgG4 against foods is not recommended as a diagnostic tool: EAACI Task Force Report. Allergy. 2008;63:793-796. http://www.ncbi.nlm.nih.gov/pubmed/18489614

DC do not recognize Ag. Just process or present. If one use a peptide, there is no processing, but binding on DC surface with MHC. If there is a bigger molecule, then the processing is involved and then peptides will be presented on the surface as MHC-peptide complexes. Everything depends on the question asked: check the processing or presentation. Activation might be involved if some Ags are processed.

Elevated IgE causes no symptoms. Elevated IgE is a result of a process such as an allergic response to multiple allergens or a mutation such as STAT3. The high IgE's seen in eczema or Hyper IgE Syndrome are an epiphenomen, not the cause of symptoms.

You are right, there are.

Some of the formulas are obscure, and the manufacturers do not declare their complete presence, but these chemicals are mostly related with skin allergies or irritations not melanoma. regards

Unfortunately, the vast majority of Hungarian physician's believe and use it. :(

Thank you and most appreciate Beatrice for your kind references.

Best regards - Mariam

I have not worked with FITC model. But generally for each mice you require 40 ul (20ul to each ear) and 40*6=240 ul for each group. Considering you have 3 groups you need 240*3=720 ul. If you consider dead volume and wastage, at least 1 ml you need to prepare per study. So you can easily weigh 5 mg and dissolve in 1 ml of vehicle.

Hope it is useful

Nagaraj

Elevated Tryptase level and not it's dcrease  is important in diagnosis of mast cell activation disorders .Therefore decreased level of tryptase has no clinical importance.

I have been interested for years in chitosan and tried to find an hypothetical role in food allergy.

I was trying to find evidence of the role of intestinal permeability changes in what now has been called “cofactror enhanced food allergy” (CEFA).

The role of chitosan as a permeability enhancer led me to investigate in its potential role in food allergy, not only as a cause of allergic reactions in shellfish allergic subjects but also as a “cofactor" as an intestinal permeability enhancer. I am less interested now, as I have not found evidence (in the literature) of its role in food allergy, but I am aware of three papers that , without solving the question, and with conflicting results, may be of interest for you:

1. Kato Y, Yagami A, Matsunaga K. [A case of anaphylaxis caused by the health food chitosan.]. Arerugi 2005; 54:1427-9.1.

   The authors report a case of immediate chitosan allergy but they not mention shellfish allergy at all. They also mention cases of delayed reactions to chitosan containing- creams

2. Waibel KH, Haney B, Moore M, Whisman B, Gomez R. Safety of chitosan bandages in shellfish allergic patients. Mil Med 2011; 176:1153-6.

    Ten shellfish allergic subjects were tested with chitosan powder skin tests and challenged with chitosan bandages and all were negative. It is a small sample but is probable the best information on the topic.

3. Bae MJ, Shin HS, Kim EK, Kim J, Shon DH. Oral administration of chitin and chitosan prevents peanut-induced anaphylaxis in a murine food allergy model. Int J Biol Macromol 2013; 61:164-8.

   The authors suggest a preventive role for peanut food allergy in a murine model, as suggested in the interesting paper that you cited.

Dear Dear Michael.

Hope everything is well with U.

In accordance with/Adverting to Alima Akhunova's  and the other friend's good recommendations, with the exception of  some negligible helpful effects in terms of psychological/aversion views, as well as, inhalation  issues,  surely, the wearing of a surgical mask is not protective/guarantying and of course, more appropriate dealing-instruments e.g. EpiPen and, additional avoidance are warranted.

you can lyophilized the cultures 

That is a very intriguing question that I am afraid we have no good answer at this point. I have not seen a study describing in details how the stoichiometric changes of the IgE molecule occurred in binding on to natural allergens or recombinent allergens as yet.

Regardless, even the results of IgE binding to a natural allergen or its recombinant allergen looks very close, at least for some allergens, especially foods or allergens to be included in allergy vaccine for immunotherapy (allergy shot) would be eventually tested in man. For instance, genetically altered food (say modified peanut) would be tested in vivo to see if allergic patients could tolerate it or not. Likewise, the effect of recombinant allergens for immunotherapy would be tested if patients symptoms would get better or not. In other words, no matter how IgE is bound to allergen, the final test would come after a real challenge in vivo is conducted..

As far as IgE-mediated hypersensitivity to insulin is concerned, four strategies of treatment are available: 1) sostitution of inslin with another kind of insulin formulation  tolerated by the patient investigated by skin tests and ImmunoCap for insulins; 2) keep patient desensitized through the placement of an infusion pump, 3) desensitization strategy with various protocols,  and, recently, the use of Omalizumab (anti -IgE agent )

I imagine you no longer want to pursue this plan? If you do, most aerobiologists obtain funding from research grants, or from government grants (for Air Quality studies). Sometimes pollen counts are essential when testing new medication i.e. nasal sprays, eyedrops. 

the patient has documented nickle allergy by both patch test and fin test

she was already on clopidogrel when she started to complain from this manifestation

she also had an intensive course of antihistaminic and steroids after consulting an immunologist but was not able to relieve her symptoms and she is refusing the idea of surgically extracting the device

The alpha-gal is a sugar that bounds to proteins, changing their allergenicity. It is more probable that the tick enzyme sensitizes the immune system in order to create a cross-reaction  sensitization to other similar alpha-gal epitopes, that produce the allergic reactions.

Even though an IgE level exceeding 100kU/l is highly suggestive of allergy in adults, the total IgE is not an accurate parameter.Total IgE may also be raised in parasitic infections, immune diseases, cigarette smokers, with alcohol consumption, certain cancers...Moreover, frequently, the presence of cross-reactive IgE antibodies is not correlated with the development of clinical respiratory or food allergy. In particular, regarding the clinical relevance of sensitization to cross-reactive carbohydrate determinants (CCD) those sensitize approximately 10-20% of all pollen-allergic patients. Therefore, the diagnosis of type 1 hypersensitivity is mainly based upon an anamnesis and clinical history and in vivo skin prick tests. Then, in vitro detection of specific IgE against sensitizing molecular allergens can be performed using either commercial procedures in single or multi-array (quantitative) or immunoprint after separation of proteins from the suspected allergenic source by electrophoresis (qualitative). Regarding the pollen allergy, the level of specific IgE may considerably increase during the pollen season...

Pediatrics. 1998 Dec;102(6):E68.

Differences between child and parent reports of symptoms among Latino children with asthma.Lara M1, Duan N, Sherbourne C, Lewis MA, Landon C, Halfon N, Brook RH.

The epub version has the questionnaire. Interestingly, the children with the least asthma had the parents who were the most afraid their children were going to die;the converse was true as well.

Dear Rajiv, the pollen of Pinus is among the most recognisable pollen grains you can capture with a spore-trap. Which kind of spore-trap you use? Probably you have trapped also other pollen grains, including Pinus pollen you can observe with microscope in other views.

There is some good evidence about direct stimulation of Mast cell and basophil of allergic patients without needs of conjugation but I do not know if it could help you

Thanks to Jana for raising this point which is likely to take on a dramatic relevance well beyond the limits of an alimentary intolerance. Recent findings have evidenced (also reported in papers listed in my RG profile) that the alpha-Gal epitope is present in most bioprosthetic products of animal origin, particularly in life-saving devices like bioprosthetic heart valves. This epitope is already widely considered as a critical factor related to the limited durability of such substitutes. However what's happening in the specific case of transplanted individuals having already a significant amount of such IgE, in addition to the natural content of IgG antibodies to this oligosaccharide? Could this situation be related to early bioprosthetic failures and/or to the less than the average durability of these devices? At the present no such investigations are apparently been carried out and are urgently expected as well as the removal of such life threatening components from the devices available for bioprosthetic purposes ..

SIT may be a short for "Subcutaneus Immunotherapy" , or "Specific Immunotherapy", we found both uses, but as the majority of americans does nor perform SLIT (sublingual immunotherapy), usually SIT refer only to the subcutaneus IT. sometimes we found SCIT to refer to "subcutaneus immunotherapy".

The effect of BSA on "most" cells are generally benign, especially in the concentrations used. But to be absolutely sure that you don't have an effect you should use a vehicle control to make sure that BSA does not have an effect on the cells.

There ARE effects of BSA on the cytokines however. We use some IL-6 family cytokines and BSA of some formulations can have adverse effects on our cytokine activity, so in some cases, we avoid using BSA. So you should first test with BSA free aliquots and compare it with aliquots containing BSA to make sure BSA does not affect your cytokine. We are not sure of the mechanism why sometimes it interferes, but we suspect that since some of our proteins are very sticky, it may bind to BSA in a manner that reduces it's receptor binding potential. Other times we found out that our supposedly Igg-free, protease free BSA has some protease activity and chews up our protein that we want to preserve. So we mainly buy from Jackson immunologicals and get their IGG and Protease free BSA, filter sterlize, and we never have had any problems since. Sigma Aldrich also sells cryoprotectant formulations with BSA added specifically for long term storage of proteins and antibodies as well.

Skin is a major absorber of whatever is put onto it so fructose containing skin products may possibly cause a reaction if fructose intolerant. There may be cross reaction with other ingredients. By the concept of total toxic load, combination of inflammatory response from fructose if intolerant together with other chemical sensitivities may be the tipping point. Possibly check fasting insulin as well.

The clinical studies based on the use of recombinant allergens do not seem to support the hypothesis that they could be of more benefit in respect to traditional immunotherapy products. Considering the huge investments to be made for their development, I don't think that recombinant allergens, at least as native ones, will be used in the future. Mutant recombinant allergens (with reduced IgE-reactivity) could be a potential alternative. They could be safer and more effective because used at higher dosages but it remains to solve the economic impact needed to develop them. Perhaps if some Allergen Producers decided to join their efforts, such products could be a future.

Yes, there is a minimal number of IgE requested to induce an allergic reaction: of the total 500,000 to 1,000,000 IgE antibodies present on the mast cell surface, only a threshold number of about 2,000 bridged IgE antibodies are required for degranulation and mediator release. This number of bridges might be possible to accumulate by more than one non-cross-reactive antigen and its corresponding IgE antibody; therefore, patients simultaneously exposed to several antigens experience more symptoms than monosensitized patients as showed by studies of Johansson (Allergy. 2006 Nov;61(11):1366-8).

CysLTr1 is typically thought to be more highly expressed in the lung, versus cysLTr2. Perhaps this is why drugs like Montelukast have been developed as antagonists. However, there has been much work done in recent years showing cysLTr1 and cysLTr2 interactions. Check out Boyce's article about this. (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2200919/). CysLTr2 plays a similar role as cysLTr1, binding cysLTs that are synthesized de novo from cells like mast cells and eosinophils and acting as bronchoconstrictors and in cell signaling. It seems there has not been a definitive work showing that cysLTr2 has obvious functional differences than cysLTr1, at least in people. Also, as a head's up, there is a third cysLT receptor, known as GPR17. Check out this article, http://www.ncbi.nlm.nih.gov/pubmed/19561298. It seems that these receptors, and their interactions, are all interrelated, and no one cysLT receptor can be given a solid role without considering the contribution of the others.

Hope that helps a bit!

Toby

Dear Joost ,

A specific IgE alone does not make an allergy diagnosis, unless it is backed up by family history and clinical symptoms, as well as allergy reaction provoked in real life by the respective allergen.But even if all that fits, a specific IgE may still not be the proof of a specific allergy since a patient may have specific IgE antibodies that do no harm( for example anti cow's milk IgE in adults) and on the other hand , one can be very allergic but have no specific IgE to any allergen ( his antibodies might sit on IgG sub classes).

Hence the final conclusion of allergy , yes or no, should be driven by an allergy specialist.

Indoor Biotechnologies markets a recombinant Der p 2 specific IgE. This antibody is a construct of mouse monoclonal anti-Der p 2 with human Fc epsilon heavy chain. The 2B12IgE functions as a human IgE antibody and is monoclonal. See: http://inbio.com/UK/Products/Antibodies/Mouse-Human-Chimeric/Mouse-anti-Der-p-2-human-IgE?cPath=& Product Code is CH-1. Our company has also recently released a multiplex arrays for measuring IgE ab on the Luminex xMAP system: IgE-QBA. The array measures IgE to 11 allergens, as well as total IgE. http://www.inbio.com/UK/Products/IgE-QBA

Yes i have seen number of cases

This question comes down to the type of DC that is presenting the antigen. e.g., if the DC picks up the antigen in an TH2 milieu and travels to a regional LN then it would drive TH2 differentiation. The cytokines of which- e.g., IL-4 and IL-13 can drive B cell isotype switching to IgE. However, in a bacterial infection, these antigens will activate the DC to present to T cells making TH1 cells and the cytokines of which (e.g, IFNy can drive IgG synthesis from B cells and make opsinizing Abs to clearance of the pathogen). Again these DCs would have a TH1 promoting phenotype in order to influence of the differentiation of the T cell that they are presenting too.

Short answer- the phenotype of the DC (depending on the cytokine milieu in gets the antigen in) determines the subsequent differentiation of the T cell and therefore where or not you make IgE (allergy) or IgG (infection control)

Hello,

please, be careful about some of the advices above, as the biological facts are ok, but an aerosolization or nebullisation of HDM is a bad idea, unless you have a very safe cabinet to do allergen exposure. These protocols were established (nebullisation/aerosolization) for Ova, a protein with low intrinsic sensitization capacity. This is not the case of HDM! HDM can sensitize with a single i.n. administration, so imagine what it can do on you or your co-workers.

You might say that I am biased about this (I work in this lab), but the way to go for HDM is according to the protocols of the lab from Bart N Lambrecht who developed these models years ago. (see a late publication: PMID: 23352232 or the paper that Frank Kirsten told you).

The concerns that you might have:

HDM as a whole extract or DerP1 alone?

Der p1 is the mose immunogenic protein of the extract, but no the only one. Accordingly, we found the sensitization to be far less effective with Der p1 alone.

Also, no one is exposed to Der p1 alone... So unless you want to work on the capacities of just this allergen, or work on a specific desensitization, the whole HDM extract is more advisable.

Method of sensitization:

i.p., i.n.? The best model is the most physiologic. I do not remember anyone injecting themselves with an allergen in order to become allergic. So unless you want to decipher the mechanisms behind i.p.-mediated immunization, i.n. is the way to go.

Tricks: When you read a paper, remember that the quantity of HDM that they use (1 ug, 1 mg...) is always (or should always be) the protein weight. Keep that in mind when you prepare yours... There are 2 weights on the bottle: Whole extract weight and protein weight.

Not all lots of HDM have the same potency for a reason or another. The doses that I recommend below will get you to about 60% eosinophilia on d14. If you get more than that, think of reducing your sensitization dose.

In brief:

Sensitization: d0, i.n., 1 ug HDM in 40 ul PBS.

Challenges: 5 consecutive days: d7-d11: 10 ug HDM in 40 ul PBS.

Sacrifice on d14 for normal BAL and mLN investigation.

You can contact me if you need more information!

Good luck!

Thanks for your comment Sven. It is true that the amount of final azide will be low but since our mice are very difficult to obtain and mantain I can not afford to try it..I would need to know that somene is using it without problems.Thanks a lot!

Hi Daisy:

I agree with the points that Michael has provided. I have been actively involved in allergy drug development for a number of years. Both of these products are approved for temporary use to relieve symptoms of allergic conjunctivitis. While these products are generally safe to use for longer periods of time, they are used primarily used to treat short-term, seasonal conditions that generally are less than 3-4 months in duration (tree, grass, mountain red cedar, ragweed pollens, and fall moulds) or pink eye. With longer term usage, you may encounter class side effects associated with antihistamines in general (i.e. rebound, and very rarely keratitis). I would also be concerned with using the same bottle for a long period of time. The tip and the solution may become contaminated with bacteria and mould, which when introduced into the eye, will cause an infection. Both products are also classified as a Category C medications which restricts usage in pregnant or beast feeding mothers. Also, please note Michael's response with using these products with contact lenses. These products should not be used with contact lenses, especially the newer silicon based long-term lenses as the preservatives used may be absorbed by a soft contact lens and effect wearability. I do not know what the drug-drug interactions are with using these products with other ocular products used to treat conditions such as glaucoma or with using with a NSAID eye drop after cataract surgery, but wonder if this may be part of the max usage time. This may be something to consider.

Dear Reza,

If you like to use mice why not DEREK mice? In these mice all Foxp3+ cells are fluorescent and all Foxp3+ Treg can be depleted by one injection of diphtheria toxin. See:

Absence of Foxp3(+) Regulatory T Cells during Allergen Provocation Does Not Exacerbate Murine Allergic Airway Inflammation. Baru AM et al. PLoS One. 2012;7(10):e47102.

If you like to transfer the results into the human system you can use a simple humanized mouse system together with gp120 for polyclonal Treg activation.

See:

CD4-mediated regulatory T-cell activation inhibits the development of disease in a humanized mouse model of allergic airway disease. Martin H et al. J Allergy Clin Immunol. 2012 Feb;129(2):521-8.

Best regards!

This is a very complicated question that several researchers are focusing their entire careers on, so I certainly don't think there's an easy definitive answer. There are a number of compelling hypotheses that come to mind:

Some version of the hygiene hypothesis, which suggests that increased exposure to pathogens, particularly helminths, in developing countries/rural populations results in the development of regulatory cells that help to reduce allergies.

Vitamin D deficiency, which is more prevalent in urban populations in developed countries, has been associated with the severity of allergic diseases and proposed to be a major factor.

Commensal microflora have been found to contribute to systemic immune effects, and differences in the microbiota arising from geographical/dietary/antibiotic usage differences have been proposed to affect the incidence of allergies.

As with most scientific hypotheses, in the case of all these hypotheses some studies have provided supporting data while others have reported opposing data.

Dear Sergey,

Thank you for your comment!

I'm worried about the steric hindrance, too.

Rio

It is difficult to give a simple answer because the question is quite imprecise and the topic very complex.

If the question is about the natural history of food allergy in children, one of the possible interpretations of the question, an answer could be like this one:

It is assumed than milk allergy is usually outgrown soon, in most cases by the age of five, egg white later, about seven years of age (egg-yolk is not usually a problem in children, except in the so called "bird-egg syndrome") and nut allergy, specially peanut allergy in the USA and UK frequently remains for life (about 20% of patients outgrow its allergy). But nut allergy is by far a more complex issue.

New data is challenging previous information with not so good prognosis for milk allergy and not so bad for peanut allergy.

A very good review of food allergy and natural history can be found in the "Guidelines for the diagnosis and management of food allergy in the United States: report of the NIAID-sponsored expert panel" JACI 2010:

http://www.jacionline.org/article/S0091-6749%2810%2901566-6/abstract

Other issues to take into account are active treatment of food allergy (immunotherapy or oral desensitization...) that may change the natural history of allergy, see for example: "Oral Immunotherapy for Treatment of Egg Allergy in Children" NEJM 2012: http://www.nejm.org/doi/full/10.1056/NEJMoa1200435

Also important could be the relevance in the prognosis of sensitization to foods at the allergen and epitope level, that could have clues for the prognosis of allergy See for example: "Specificity of IgE antibodies to sequential epitopes of hen's egg ovomucoid as a marker for persistence of egg allergy" Allergy 2007: http://onlinelibrary.wiley.com/doi/10.1111/j.1398-9995.2007.01332.x/pdf

There are many more issues, may be, these ones can help you

Why u need monoclonal antibody for dustmite, u can get specific response with prick test just u need the dustmite allergen., which is very cheap.