Intestinal anaphylaxis: mediation of the response of colonic longitudinal muscle in rat.

Colonic smooth muscle function may be altered in food protein hypersensitivity reactions and could contribute to the clinical manifestation of diarrhea. To characterize such functional changes and elucidate the mediators and mechanisms involved. Hooded-Lister rats were sensitized by intraperitoneal injection of egg albumin (10 micrograms), and controls were sham sensitized with saline. Fourteen days later the contractility of longitudinally oriented distal colonic segments (mucosa intact) were studied in standard tissue baths in response to antigen (Ag) or other agents. After Ag exposure, a contractile response was documented in animals that were sensitized [specific immunoglobulin E (IgE) antibody levels > or = 1:64] and was specific for the sensitizing Ag. Mast cell involvement was suggested by a significant reduction in the number of granulated mucosal mast cells in sensitized tissues after Ag challenge and in the magnitude of the Ag-induced contractile response in the presence of mast cell stabilizers. The antigen-induced response was significantly and independently inhibited by both cyclooxygenase and lipoxygenase enzyme inhibitors and by leukotriene D4 and platelet activating factor receptor antagonists. The Ag-induced response was resistant to histamine and the 5-hydroxytryptamine antagonists, atropine and tetrodotoxin. These results suggest that the food protein-induced contraction of colonic longitudinal smooth muscle in the sensitized rat is due to IgE-mediated mast cell activation with the subsequent production and release of membrane-derived mediators that, in vitro, act directly on the smooth muscle.