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(Journal of Leukocyte Biology. 2002;71:1005-1011.)
© 2002 by Society for Leukocyte Biology

Regulation of cyclooxygenase-2 by nitric oxide in activated hepatic macrophages during acute endotoxemia

Nosheen Ahmad, Li C. Chen, Marion A. Gordon, Jeffrey D. Laskin and Debra L. Laskin

Rutgers University and University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway

Correspondence: Debra L. Laskin, Rutgers University, 160 Frelinghuysen Rd., Piscataway, NJ 08854. E-mail: laskin{at}eohsi.rutgers.edu

Eicosanoids generated via cyclooxygenase-2 (COX-2) and nitric oxide produced from inducible nitric oxide synthase (NOSII) have been implicated in endotoxin-induced tissue injury. In the present studies, we characterized COX-2 and NOSII activity in rat hepatic macrophages and their interaction during acute endotoxemia. Kupffer cells from control animals were found to constitutively express COX-2 and NOSII mRNA and protein. Whereas treatment of the cells with lipopolysaccharide (LPS) and/or interferon-{gamma} (IFN-{gamma}) had no major effect on COX-2, NOSII expression increased. Induction of acute endotoxemia resulted in a rapid and transient increase in constitutive COX-2 expression and prostaglandin E2 (PGE2) production by liver macrophages as well as NOSII expression and nitric oxide release. Cells from endotoxin-treated rats were also sensitized to generate more nitric oxide and express increased NOSII in response to LPS and IFN-{gamma}. Inhibition of NOSII with aminoguanidine reduced COX-2 mRNA and protein expression as well as PGE2 production by activated macrophages from endotoxemic, but not control animals. In contrast, SC236, a specific COX-2 inhibitor, had no effect on NOSII mRNA or protein levels or on nitric oxide production by hepatic macrophages, even after endotoxin administration. These data suggest that activation of COX-2 may be important in the pathophysiological response of hepatic macrophages to endotoxin. Moreover, nitric oxide is involved in regulating COX-2 in activated liver macrophages during acute endotoxemia.

Key Words: PGE2 • NOSII • liver • Kupffer cells




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