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Revisiting the "hygiene hypothesis" in gastrointestinal allergy.

The "hygiene hypothesis" in its original form hypothesized that infection in early childhood acquired through unhygienic contact with siblings or the mother may prevent the development of allergic disease. Several recent epidemiologic surveys showing an inverse relationship between the frequency of infectious disease and the incidence of allergic diseases lend support to this hypothesis. Allergen sensitization of the immune system can occur early in utero against a background of neonatal commitment to a Th2 immune response involving the production of Th2 cytokines (eg, interleukin (IL)-4, IL-5, IL-13) that are the principal mediators of allergic inflammation. Continued allergen exposure is associated with predominantly CD4+ Th2 cell proliferation but does not exclude a minor Th1 allergen-specific subpopulation that can be further expanded nonspecifically and polyclonally by microbial superantigens or as bystanders, by interferon-gamma (IFN-gamma) and IL-2 released from Th1 effectors responding to antigens associated with infectious pathogens. Th1 cytokines can also subvert allergen-specific Th2 lymphocytes to become allergen-specific Th1 cells-a process reminiscent of the increased tendency of the maturing immune system of growing adults to mount a Th1 response to some environmental and dietary antigens. Unlike Th2 cytokines, IFN-gamma and IL-2 inhibit B-cell production of IgE and, hence, delimit the capacity of mast cells to degranulate and release allergenic mediators. The ability of infectious agents through their danger signals to initiate a Th1 response that deviates the Th2 allergenic bias is the basis of the hygiene hypothesis.