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Concurrent exposure to thermal stress and oral Ag induces intestinal sensitization in the mouse by a mechanism of regulation of IL‐12 expression
Author(s) -
Liu Tao,
Wang BinQuan,
Wang ChangSheng,
Yang PingChang
Publication year - 2006
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/j.1440-1711.2006.01452.x
Subject(s) - sensitization , mechanism (biology) , microbiology and biotechnology , chemistry , biology , immunology , physics , quantum mechanics
The mechanism of food allergy remains unclear. The absorption of intact protein Ag into the intestinal tissue is a prerequisite in the development of intestinal sensitization. Previous studies indicate that thermal stress compromises the intestinal barrier function. Mice were concurrently exposed to thermal stress and oral Ag. Intestinal sensitivity, levels of serum‐specific IgE, IL‐4 and INF‐γ were assessed. Intestinal dendritic cell, Th1 and Th2 functions were determined. The mice that were treated with thermal stress and oral Ag showed high levels of serum Ag‐specific IgE, intestinal mast cell activation in response to oral Ag challenge, suppression of IL‐12 expression in the intestinal dendritic cells, inhibition of T‐bet expression and Th1 function and marked increases in (GATA) 3 expression and Th2 function. Mice exposed to thermal stress alone or oral Ag alone did not show any signs of the intestinal sensitization. Pretreatment with IL‐12 inhibited the intestinal sensitization induced by the concurrent exposure to thermal stress and Ag gavage. We conclude that although Ag absorption is essential, Ag absorption alone is insufficient; other accessory factors that can disturb the local immune homeostasis are also required for the induction of intestinal sensitization. The present study illustrates that concurrent exposure to thermal stress and oral Ag can prove to be a factor in the induction of intestinal sensitization by a mechanism of regulating IL‐12 expression.