Sulphydryl blocker-induced rat colitis is ameliorated by intravenous injection of antibody to colonic surfactant-like particle

A rat model of experimental colitis and jejunitis induced by iodoacetamide (IA), a sulphydryl blocker is accompanied by increased leukotriene, prostag landin E-2 (PGE(2)) generation, and nitric oxide synthase (NOS) activity. R at small intestinal and colonic surfactant-like particles (SLP) that accumu late on the apical surface of mucosal cells have been identified and specif ic antibodies to them have been produced. The aim of this study was to eval uate a possible role of SLP in IA-induced colitis and jejunitis. Inflammati on was induced in Sprague-Dawley rats either by intracolonic administration of 3% IA (0.1 ml) or by intrajejunal administration of 2% IA (0.1 mi. Anti sera raised against either colonic SLP, pulmonary SP-A ia major protein ass ociated with colonic SLP), or small intestinal SLP were injected into the t ail vein of rats 48 h before, simultaneous with, or 24 h after IA administr ation. Rats were killed 2 or 10 days after IA was given, their colon or sma ll intestine was isolated and rinsed, and a segment of colon (10 cm) or sma ll bowel (30 cm) was weighed and processed for microscopy, NOS and myeloper oxidase (MPO) activities, and PGE(2) generation. Intracolonic or jejunal IA resulted after 48 h in extensive macroscopic and microscopic damage, accom panied by increased segmental weight, MPO and NOS activity, and PGE(2) gene ration. Colonic SLP antibody administration, either 48 h before or at the t ime of damage induction, significantly decreased macroscopic as well as mic roscopic damage, segmental weight, MPO activity, and PGE(2) generation, but had no effect on NOS activity. Neither control sera nor antisera against S P-A had any protective effect, nor did injection of anti-colonic SLP antise ra given 24 h after IA. Small bowel SLP antibody offered no protection agai nst IA jejunitis, IA-induced colitis but not jejunitis is ameliorated by in travenous injection of SLP antibody by a mechanism yet to be determined. Th ese data provide further evidence of a physiologic role for gastrointestina l SLP.