# IgE, allergies and parasite infections



## Guest (Mar 24, 2001)

As you can see, I'm on a "parasite" kick tonight...







---------------------------------------------Immunol Cell Biol 1996 Aug;74(4):337-45 IgE, allergies and helminth parasites: a new perspective on an old conundrum.Bell RGDivision of Biochemistry and Molecular Biology, John Curtin School of Medical Research, Australian National University, Canberra Australian Capital Territory, Australia.This paper analyses the association between infection with helminth parasites, the elevated production of IgE and the expression of allergies. Interpretations of this interaction have taken place in a scientific environment whose most secure element is the immunochemistry of allergic reactions resulting in a substantial body of literature that has sought a biological role for allergic reactivity in protective immunity directed against helminth parasites. While the association between helminth infections and elevated levels of IgE, mast cells and eosinophils is well established, a functional role for allergic reactions in protection against helminths has eluded experimental proof. Instead of this hypothesis, it is proposed that allergic reactivity is rarely present in helminth-infected individuals because allergic reactions do not function to regulate helminth infections. Data from many sources are used to establish that the 'normal' state of all mammals is to be infected with helminth parasites from shortly after birth until well into adulthood. Only in the last 100 years or so have people living in areas of high development with sophisticated water and sewage systems been able to escape helminth infection. Allergies are as conspicuously present in these human populations as they are absent in populations that are still regularly exposed to helminths. Furthermore, in populations with endemic helminthoses there is little overt expression of allergic pathology that could be connected to the acquisition or elimination of helminth parasites. Based on these observations, it is suggested that endemic helminthoses activate the Th2 system, particularly at mucosal surfaces, to provide a different level of immunological homeostasis than currently occurs in developed societies. Under these conditions, mast cells, eosinophils and IgE rarely participate in reactions that we would recognize as 'allergic', although their participation in the control of helminth infections is still envisaged. Allergic reactions are considered to be a purely pathologic consequence of the disruption of this homeostatic mechanism and are not protective at all for the individual expressing them. This interpretation is derived from the immunobiology of the host-parasite interaction rather than the biology of allergies and should lead to new concepts regarding both allergic disease and the role of helminth infections in human and animal populations.


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## Mike NoLomotil (Jun 6, 2000)

Comments for other readers of the post, as the language is even denser than my ownarasites are a set or organisms that are unicellular (protozoans) up to multicellular invertebrates (such as the helminths, whch are intestinal worms and the blood, liver and lung flukes). They are much larger than normal microbial pathogens, and since they cannot be phagocytized they canot be managed by the normal cellular and molecular immune responses. So the immune system developed a different startegy, based on IgE.In those populations where exposure to to parasites, including helminths, is common and expected their abilty to infest the host is controlled by the IgE mechanism which is used (through a specific mechanism related to the mast cell FceRI receptors) to sensitize a the mast cells for various specific antigens. In this population the antigens mast cells are "set" to included guarding against specific parasites, which would include the helminthic population they will be exposed to indigenously in that region.So, with the mast cells sitting there preloaded (IgE tightly bound to the Fc-to-FceRI-of the mast cells), when a parasite gets into the gut (or lung) the mast cells degranulate and release inflammatory mediators in massive amounts which set in motion the "evacuatory reponse". Further,some parasites which become "coated" with IgE then elicit an eosinophilic reaction....and the eosinophils will attach to the parasite and inject it with chemical mediators to kill it.So this is all part of normal IgE function and in populations where people are exposed to parasites IgE is busy playing its role as are the mast cells. So environemntal allergies or food allergies, where IgE has sensitized mast cells to harmless substances like pollen or shellfish. Conversely in populations where parasites are rare, "allergy" is much more pronounced. This is basically what this summary is saying.Now since 1996 a lot of new work has been done, especially in Sweden, studyin the mucosal reponse (mast cell) in the gut attempting to understand beter WHY BOTH IgE specific food allergy response of the mast cells AND NON-IgE mediated responses of the small bowel mast cells occur in response to innocuous subatnces like foods.One of the more interesting findings besides proving this phenomenon (that the mast cell response can and does occur in patients who are TEST NEGATIVE TO IgE but ORAL CHALLENGE POSITIVE) is that the reaction is not limited to the cllular response in the gut microvasculature as has been suspected, but small bowel mast cells as well, pointing the way to either localized IgE or another mechanism for triggering mast cell response or both. One finding is CD1 sensitized sites in the lamina propria indicating the alternate-pathway complement response is involved in these food-reactive people which is not the case in non-reactive people (no CD1 seen or minimal). So the full understanding of WHY IgE mediated systems designed to protect against parasits malfunctuion in some peopel when there are no parasites to protect against is still not fully elucidated but progress is being made.MNL_____________ www.leapallergy.com


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## Guest (Apr 3, 2001)

More recent work on the influence of parasite infections on allergic responses...---------------------------------------------J Allergy Clin Immunol 1998 Feb;101(2 Pt 1):217-21 Relationship between helminthic infection and IgE response in atopic and nonatopic children in a tropical environment.Lynch NR, Hagel IA, Palenque ME, Di Prisco MC, Escudero JE, Corao LA, Sandia JA, Ferreira LJ, Botto C, Perez M, Le Souef PNInstituto de Biomedicina, Universidad Central de Venezuela, Caracas.[Record supplied by publisher]BACKGROUND: Although IgE antibody is clearly involved in allergic reactions to environmental allergens, this immunoglobulin is an important component of host-protective immune responses against the helminthic parasites that are endemic in the majority of the world population. However, these infections not only stimulate the production of antiparasite IgE antibody but can nonspecifically induce polyclonal IgE synthesis that results in highly elevated total serum IgE levels. Such polyclonal stimulation can diminish specific IgE antibody responses and cause saturation of mast cell Fc epsilon receptors, thus inhibiting allergic reactivity. This may represent a mechanism of immune evasion by the parasite. OBJECTIVE: Because an atopic disposition is generally recognized to be associated with elevated IgE synthesis against environmental allergens, the aim of this study was to evaluate the influence of atopy on the antiparasite response. To this end, we examined two groups of Venezuelan children in whom the intestinal helminth Ascaris lumbricoides is endemic but that differ greatly in their level of atopy. One group was from an island population (Coche Island) that has a very strong atopic background and in which the prevalence of allergic disease is extremely high. The other was a group of nonatopic children belonging to a mainland population (Barrio Los Erasos) that is of comparable socioeconomic level and has an exposure to helminthic infection similar to that of the island group but a relatively low expression of allergic diseases. RESULTS: Although the living conditions and the prevalence of Ascaris infection of the two groups were comparable, the intensity of the parasitic infection was considerably higher in the nonatopic mainland children (geometric mean values of eggs per gram of feces: Barrio Los Erasos, 7621; Coche Island, 1435; p < 0.001). In addition, their total serum IgE levels were significantly more elevated than in the atopic island group (geometric mean: Barrio Los Erasos, 2172; Coche Island, 941 IU/ml; p < 0.001). In contrast, the specific anti-Ascaris response was much stronger in the atopic children (geometric mean: Barrio Los Erasos, 0.30; Coche Island, 0.91 PRU/ml; p < 0.001), which resulted in the ratio of specific to total IgE being nine times higher than in the nonatopic mainland subjects. These differences were maintained even when the children were matched on the basis of infection intensity, thus indicating that the atopic children have an intrinsic propensity to favor specific over polyclonal IgE responses to the parasite. CONCLUSIONS: The children with a strong atopic background demonstrated IgE responses concordant with an enhanced protective response against helminthic parasites and had significantly lower intensities of infection than their nonatopic counterparts. These observations support the concept that the atopic state has conferred a selective evolutionary advantage that could compensate for its involvement in allergic disease.---------------------------------------------The authors note an inverse relationship between allergic frequency and the degree of parasite infection in Venezuela. Of those subjects with light worm infections, 43% had allergies. These subjects lived in homes with running water and toilets. By contrast, Venezuelan Indians who lived in the rain forests had very high rates of parasite infection (88%), but no allergies. Interesting stuff, eh?


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## Mike NoLomotil (Jun 6, 2000)

This understanding of the inverse relationships between frequency in a population of parasite exposure vs. incidence of atopy was established a long time ago. This realationsjip is a standard inclusion in basic immunology textbooks, where they explain how the function of IgE was developed. It is interesting that some investigators keep revisiting an already well beaten path, though.MNL_______________ www.leapallergy.com


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