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Am J Physiol Gastrointest Liver Physiol 275: G467-G472, 1998;
0193-1857/98 $5.00
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Vol. 275, Issue 3, G467-G472, September 1998

PAF and CD18 mediate neutrophil infiltration in upper gastrointestinal tract during intra-abdominal sepsis

A. James Beyer1, David M. Smalley1, Yi-Ming Shyr2, John G. Wood1, and Laurence Y. Cheung1

1 Departments of Surgery and Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, Kansas 66160; and 2 Department of Surgery, Veterans General Hospital-Taipei, National Yang Ming University, Taiwan 11217, Republic of China

Neutrophil infiltration is a critical event in the development of multiple organ failure during sepsis. We hypothesized that platelet-activating factor (PAF) release contributes to neutrophil infiltration in the gastrointestinal tract during sepsis. In the first experiments we administered exogenous PAF (1.56, 6.25, 25, and 100 ng · kg-1 · min-1 for 30 min) to urethan-anesthetized Sprague-Dawley rats. PAF was administered alone or in combination with either the PAF antagonist WEB-2086 (250 µg · kg-1 · min-1), a monoclonal antibody (MAb) to CD18, or a MAb to intercellular adhesion molecule 1 (ICAM-1). In separate groups of rats, cecal ligation and incision (CLI) was performed to create intra-abdominal sepsis, which we hypothesized would stimulate the release of endogenous PAF. CLI was performed in rats given either saline, WEB-2086, anti-CD18, or anti-ICAM-1 MAb. After these experiments, tissue myeloperoxidase (MPO) levels were determined as a marker of neutrophil infiltration. Both exogenous PAF and CLI induced significant increases in MPO activity in the stomach and duodenum. These increases were significantly attenuated by WEB-2086, anti-CD18 MAb, and anti-ICAM-1 MAb in both PAF- and CLI-treated rats. These results suggest that both the inflammatory mediator PAF and the CD18 integrins play a major role in neutrophil infiltration in the upper gastrointestinal tract during sepsis.

cecal ligation and incision; intercellular adhesion molecule 1; leukocyte adhesion; WEB-2086


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