Increased ICAM-1 and beta2 integrin expression in parenterally fed mice after a gut ischemic insult.
Academic Article
Overview
abstract
Lack of enteral feeding increases P- and E-selectin and ICAM-1 expression on endothelial cells in organs, such as the small intestine and lung, and increases neutrophils in the intestine. These changes are associated with increased mortality after gut ischemia. We hypothesize that nutritional regimen affects endothelial ICAM-1 levels and leukocyte beta2 integrins after gut ischemia. Mice received chow, intravenous (IV) TPN, or intragastric (IG) TPN. In experiment 1, after 5 days of diet, 28 mice underwent 15 min of superior mesenteric artery (SMA) occlusion (I/R) for quantification of ICAM-1 expression in organs 3 h later. In experiment 2, after the same nutrient pretreatments of 38 mice, peripheral blood was obtained with or without gut I/R to measure CD11a and CD11b expression on myeloid cells. CD18 immunofluorescence staining was studied in the lung. Expression of ICAM-1 in the liver, kidney, and small intestine was significantly higher after IV-TPN than chow. IG-TPN reduced liver and kidney ICAM-1 levels midway between the chow and IV-TPN groups, but not intestinal expression. Expression of CD11b on the myeloid cell population in each group was similar before I/R, but CD11b levels increased after IV-TPN on circulating cells after I/R compared with all uninjured animals or injured chow or IG-TPN mice. Only IV-TPN mice had lung CD18-positive leukocytes after I/R. After I/R, lack of enteral feeding increases organ expression of ICAM-1, CD11b levels on myeloid cells, and lung of CD18 positive leukocytes. Through these changes, lack of enteral feeding may increase organ damage after gut ischemia.
