During the last few years, most of the societies, all over the world, have been facing a progressive increase of adverse reactions to food. Accordingly, as many as 20-30% of the general population, in the gross, report some two adverse reactions to food components, of which, for the most part, allergic disorders are of considerable concerns owing to their epidemic increase in prevalence and morbidity.
Taken together, allergic diseases constitute one of the major problems of modern day medicine. Currently, numerous strategies for definitive treatment are being studied, including sublingual/oral immunotherapy, injection of anti-IgE antibodies, cytokine/anti-cytokine therapies, Chinese herbal ...view middle of the document...
From chronological point of view, the Brown Norway (BN) rat is a high-immunoglobulin (specifically IgE) responder, allowing some level of comparison to atopic humans3,6.
Collectively, our evaluations in this investigation demonstrated the clinical, immunological, and pathological features of PN allergy as seen in human beings supporting the wistar rats sensitised orally, as more prone to IgE-mediated allergic-type responses and suitable model for scrutinizing the PN allergy-pertaining pathomechanisms.
But now, taking into account all of the newly achieved outcomes, we assert daringly that the wistar-strain rats resembled mechanistically, the human being-corresponding peanut allergic reactions, in a very close manner.
Sensitization is induced by following exposure of the susceptible individual to the protein allergen sufficient to stimulate an IgE antibody response. If the now-sensitized individual is exposed subsequently to the same protein, then antigen cross-links specific membrane-bound IgE antibodies and this in turn causes mast cell degranulation and the release of inflammatory mediators such as histamine, cytokine, and so on, which together initiate the symptoms of food allergy[11,12].
In summary, food allergies are common (might be increasing in prevalence), result in both acute and chronic disease, affect quality of life, and can be severe and potentially fatal.
So much is certain that our comprehensive understanding of the underlying pathomechanisms of these diseases is an urgent issue and doubtlessly will warrent the search of appropriate therapeutic approaches that can either modulate the sensitization process or impact on allergic mediators and hereby, helping manage food-allergic sequelae.
Currently, numerous strategies for definitive treatment are being studied, but, most of the clinical studies concerning these new therapies are still, performed in animal models and evidently, not all of them do necessarily offer hope for better treatments in mankind subjects. But anyhow, the need for more compatible animal models is apparent.
For an animal model to be truly of value in this context there is a necessity to understand performance characteristics and to acknowledge limitations, particularly with regard to reliability under different circumstances, all to increase our knowledge of IgE, as well as the possibility to use more suitable model in studies of IgE-mediated hypersensitivity reactions.
At present, rodent models are generally employed in studies of IgE-mediated reactions, owing in part to the availability of the reagents required to monitor the reactions. However, there are several differences between the rodent and human systems that require consideration. For instance, rodent FcεRI is expressed exclusively on mast cells and basophils and has an obligatory αβγ2 structure, whereas human FcεRI appears to have a wider distribution including eosinophils and platelets as well as monocytes, Langerhans cells and dendritic cells in a...