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Am J Physiol Lung Cell Mol Physiol 281: L537-L543, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 3, L537-L543, September 2001

EDITORIAL FOCUS
Selective inhibition of COX-2 improves early survival in murine endotoxemia but not in bacterial peritonitis

Raju C. Reddy1, Gina H. Chen1, Kazuhiro Tateda2, Wan C. Tsai1, Susan M. Phare1, Peter Mancuso1, Marc Peters-Golden1, and Theodore J. Standiford1

1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, The University of Michigan Medical School, Ann Arbor, Michigan 48109-0360; and 2 Department of Microbiology, Toho University, Tokyo 143-0015, Japan

Prostaglandins of the E series are believed to act as important mediators of several pathophysiological events that occur in sepsis. Studies were performed to evaluate the effect of cyclooxygenase (COX)-2-specific inhibition on the outcome in murine endotoxemia and cecal ligation and puncture (CLP). We observed a significant time-dependent upregulation of PGE2 production in both blood and lung homogenates of mice administered lipopolysaccharide intraperitoneally, which was nearly completely suppressed by the administration of the COX-2 inhibitor NS-398. Treatment with NS-398 significantly improved early but not late survival in lipopolysaccharide-challenged mice. On the contrary, elevated PGE2 levels were found in bronchoalveolar lavage fluid but not in plasma of mice subjected to CLP (21 gauge). Pretreatment with NS-398 failed to significantly improve survival in CLP mice. No significant differences were noted in plasma or lung homogenate proinflammatory cytokine levels or lung neutrophil sequestration between the NS-398-treated and control groups. These results demonstrate that selective COX-2 inhibition confers early but not long-term benefits without affecting the expression of proinflammatory cytokines or the development of lung inflammation.

prostaglandin E2; cyclooxygenase-2; cecal ligation and puncture; NS-398; sepsis


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