The tripeptide feG reduces endotoxin-provoked perturbation of intestinal motility and inflammation

Abstract

Lipopolysaccharide (LPS)-induced intestinal endotoxaemia perturbs motility and causes activation and influx of inflammatory cells into the muscle tissue. Because rat submandibular gland peptide T (SGP-T; Thr-Asp-Ile-Phe-Glu-Gly-Gly), its carboxyl-terminal fragment tripeptide, FEG (Phe-Glu-Gly) and its D-isomeric analogue, feG, modulate intestinal anaphylactic reactions, we examined whether these peptides also modulate LPS-induced intestinal endotoxaemia in conscious rats. The disruption of the fasting pattern of intestinal MMCs (migrating motor complexes), induced by intravenous LPS (20 microg kg-1) injection, was prevented by all three peptides. The extravasation of leucocytes into the peritoneal cavity and increased expression of the activation marker CD18 on mesenteric tissue leucocytes (18 h after intraperitoneal injection of LPS) were reduced by orally administered feG, which also significantly decreased the number of intestinal tissue leucocytes expressing the integrin CD18. We conclude that feG attenuates both the immediate (intestinal motility) and late ( approximately 18 h) inflammatory reactions provoked by endotoxaemia.