The Role of Intestinal Epithelial Cell CD23 in Food Allergy
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Date
2005-12-02
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Abstract
The incidence and severity of food hypersensitivity is increasing. Oral allergen challenge in sensitized individuals leads to a series of local events known as intestinal anaphylaxis. IgE-mediated binding of allergen and CD23 on the surface of intestinal epithelial cells, leads to transepithelial transport. Intact allergen rapidly crosses the intestinal barrier. Mast cell bound IgE-mediated recognition of allergen, leads to cross-linking, degranulation and release of mast cell mediators. These mediators with local nerves generate a chloride secretory event by the intestinal epithelial cell.
An HRP immunization mouse model of intestinal anaphylaxis was examined in Ussing chambers for response to allergen challenge. A disparate secretory response to luminal allergen challenge was observed between SPF and GF mice. CD23 expression and mast cell numbers were similar. CD23-mediated transepithelial transport was present in GF mice despite the lack of a secretory response. HRP-specific IgE was significantly lower in sera of immunized GF mice versus immunized SPF mice. Specific IgE and intestinal CD23 were adequate to allow CD23-mediated transport. Mast cell numbers also appeared adequate. Elevated circulating IgE in SPF mice is proposed to cause up-regulation of high-affinity IgE receptors on the surface of mast cells, resulting in increased sensitivity.
The colons of control and maltese x beagle dogs from a colony with naturally occurring food allergy were examined in Ussing chambers for intestinal anaphylaxis and permeability changes in response to serosal allergen challenge. Exogenous histamine caused a secretory response. A consistent secretory response was not observed in response to allergen challenge with bovine milk, whole wheat or soybean or anti-canine IgE treatment. Baseline resistance in control dogs was significantly greater than maltese x beagle dogs. Greater mannitol flux was shown in the maltese x beagle dogs during the third of four 30 minute flux periods. However, maltease x beagle dogs had significantly greater mannitol flux during the one of two 60 minute flux periods after bovine milk, doxantrazole (a mast cell stabilizer) with bovine milk and soybean allergen. Furthermore, the maltese x beagle dogs only demonstrated an increase in mannitol flux over time in response to bovine milk allergen alone and with doxantrazole. In conclusion, the maltese x beagle dogs examined did not demonstrate the secretory response to allergen challenge but did demonstrate changes in permeability in response to certain allergen. Since doxantrazole did not diminish the response to bovine milk allergen, either mast cells are not involved or it is incapable of stabilizing mucosal mast cells.
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Keywords
HRP, canine, murine, Food Allergy, Ussing chamber, CD23
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Degree
PhD
Discipline
Immunology
