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Am J Physiol Regul Integr Comp Physiol 283: R1263-R1274, 2002. First published July 18, 2002; doi:10.1152/ajpregu.00278.2002
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Vol. 283, Issue 5, R1263-R1274, November 2002

Effect of hemorrhagic shock on gut barrier function and expression of stress-related genes in normal and gnotobiotic mice

Runkuan Yang1, David J. Gallo2, Jeffrey J. Baust2, Simon K. Watkins3, Russell L. Delude1,4, and Mitchell P. Fink1,2

Departments of 1 Critical Care Medicine, 2 Surgery, and 4 Pathology and 3 The Center for Biologic Imaging, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15260

We sought to determine whether gut-derived microbial factors influence the hepatic or intestinal inflammatory response to hemorrhagic shock and resuscitation (HS/R). Conventional and gnotobiotic mice contaminated with a defined microbiota without gram-negative bacteria were subjected to either a sham procedure or HS/R. Tissue samples were obtained 4 h later for assessing ileal mucosal permeability to FITC dextran and hepatic and ileal mucosal steady-state IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, and TNF mRNA levels. Whereas HS/R significantly increased ileal mucosal permeability in conventional mice, this effect was not apparent in gnotobiotic animals. HS/R markedly increased hepatic mRNA levels for several proinflammatory genes in both conventional and gnotobiotic mice. HS/R increased ileal mucosal IL-6 and COX-2 mRNA expression in conventional but not gnotobiotic mice. If gnotobiotic mice were contaminated with Escherichia coli C25, HS/R increased ileal mucosal permeability and upregulated expression of IL-6 and COX-2. These data support the view that the hepatic inflammatory response to HS/R is largely independent of the presence of potentially pathogenic gram-negative bacteria colonizing the gut, whereas the local mucosal response to HS/R is profoundly influenced by the microbial ecology within the lumen during and shortly after the period of hemorrhage.

translocation; bacterial; permeability; mucosal; tumor necrosis factor; cyclooxygenase-2; inducible nitric oxide synthase; interleukin-6


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