Anaphylactic colonic hypersecretion in cow's milk sensitized guinea-pigs depends upon release of interleukin-1, prostaglandins and mast cell degranulation.

Abstract

The effect of beta-lactoglobulin (beta-LGI) challenge on net water movements into the proximal colon and the role of Interleukin-1 (IL-1), prostaglandins and mast cell degranulation on the challenge-induced net water changes were assessed in vivo using isolated colonic loops in anaesthetized guinea-pigs immunized to bovine milk. beta-lactoglobulin challenge infused into the colonic loop during 30 min reversed the net water flux into a net secretion during the period of antigen infusion. Doxantrazole, a mast cell stabilizing agent, administered 120 min before challenge infusion, suppressed challenge-induced hypersecretion. Similarly recombinant IL-1 receptor antagonist protein abolished the antigen-induced colonic secretory effect. Indomethacin, a prostaglandin synthesis inhibitor, administered 20 min prior to antigen infusion, significantly (P < 0.05) reduced, but did not abolish, the challenge-induced colonic secretory effect. These results suggest that IL-1 plays an important role in antigen challenge-induced colonic hypersecretion which involves mast cell degranulation and prostaglandin release.