The GI tract plays a pivotal role in the mucosal immune response. While permitting the absorption of nutrients from the intestinal lumen to the systemic circulation, the GI tract also protects the body against invasion from microbes and other antigens by inducing an immune response. Loss of oral tolerance—the decrease or down-regulation of the immune response— can result in increased local inflammation in the gut. These inflammatory reactions cause increased intestinal permeability that allows more dietary antigens access to the systemic circulation, which can lead to the development of food allergen reactivity.19 Some scientists say that this dysfunction may be caused by exposure to high doses of antigens, which override the protective mechanisms; but other scientists question if this is, indeed, a matter of dysfunction, suggesting instead that the body might normally react to high levels of exposure to antigens. Allergic reactivity to food is the result of both IgE and non-IgE-mediated mechanisms. Non-IgE-mediated allergic responses tend to involve a T-cell-mediated delayed hypersensitivity reaction, with released cytokines determining the immune response. Serum analysis of patients with immediate-type food-allergy symptoms have revealed a significant correlation between titers of antiallergen antibodies of both isotypes, indicating that immune stimulation from allergenic foods is not limited only to IgE but also affects IgG-producing antibody systems as well.20
GI symptoms in food allergy have been explained by alterations in transport across the intestinal wall (increased secretory and=or decreased absorptive functions), increased permeability, and motility of the intestine.21 In addition, repeated intestinal infections, coupled with reduced secretory IgA levels, can alter intestinal permeability and result in increased food antigen access to the systemic circulation. Such an increased antigenic load, combined with a patient's allergic predisposition, may foster immunologic responses to food proteins. It is commonly acknowledged that food comprises the largest pool of antigenic challenges to the immune system.22 Food allergy is, indeed, an important and common health issue that warrants the need to identify and characterize the sensitizing potential of food proteins.
Current approaches to identify food allergy include consideration of amino acid sequence homology with known human allergens, sequence homology with human cell-surface antigens (as is the case with numerous cereal grains and connective-tissue antigens), serologic cross-reactivity with known allergens, and quantifying resistance to proteolytic digestion. Although these concepts do not explain the ability of a protein to cause allergic sensitization, they do provide information regarding the pathogenesis of allergy. What does explain the increasing incidence of allergic symptoms? A primary cause may be repetitive consumption of high doses of similar foods such as processed wheat and corn on a long-term basis, along with ingesting food additives, such as preservatives, coloring, flavor-enhancing agents, and antibiotics.23 In addition, it has been speculated that infrequent food rotation predisposes patients toward developing hypersensitivities. Coupled with inadequate digestion of proteins into requisite amino acids, dipeptides, and short-chain polypeptides, partial proteins are able to retain their antigenic properties thereby provoking the immune system once they are allowed into systemic circulation. Early introduction of antigenic proteins may also contribute. Researchers have shown that exposure to cow's milk during the first three months of life is associated with high IgG4 subclass antibody levels to beta-lactoglobulin up to eight years of age, particularly in children with maternal atopy.24
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