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Attenuation of Intestinal Endotoxemia in Rats by the Salivary Gland Tripeptide FEG and its d-Isomeric Analog feG

Ronald Mathison (Physiology & Biophysics, University of Calgary, Canada)
Pierrette Lo (Physiology & Biophysics, University of Calgary, Canada)

Contact person: Pierrette Lo, paplo@ucalgary.ca

Abstract

Rats were used to investigate the effects of rat submandibular gland peptide T (SGP-T; Thr-Asp-Ile-Phe-Glu-Gly-Gly), its carboxy-terminal fragment FEG (Phe-Glu-Gly) and its d-isomeric analog feG on lipopolysaccharide (LPS)-induced intestinal endotoxemia. The immediate effect (within 30 min) of LPS is to disrupt the fasting pattern of MMCs (migrating motor complexes) in the intestine. There is also delayed extravasation, 18 h after i.p. injection of LPS, of leukocytes into the peritoneal cavity and increased expression of the activation marker CD18 on mesenteric tissue macrophages. feG, when administered intraperitoneally along with LPS, caused a significant decrease in the duration of disruption of MMCs compared to rats treated with LPS only. Only feG and FEG were found to have this effect; intravenous SGP-T did not. feG also caused a significant decrease in the number of mesenteric tissue macrophages expressing CD18, but did not affect the number of cells expressing the migrating and resident macrophage markers ED1 and ED2, respectively. feG significantly decreased the total number of cells in the peritoneal cavity as well as decreasing the differential counts of macrophages and neutrophils. We conclude that feG attenuates both the immediate (intestinal motility) and delayed (cellular) reactions provoked by endotoxemia.


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