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Am J Physiol Cell Physiol 282: C263-C270, 2002; doi:10.1152/ajpcell.00357.2001
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Vol. 282, Issue 2, C263-C270, February 2002

Cyclooxygenase 2-mediated suppression of macrophage interleukin-12 production after thermal injury

Martin G. Schwacha, Chun-Shiang Chung, Alfred Ayala, Kirby I. Bland, and Irshad H. Chaudry

Center for Surgical Research, Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama 35294; and Division of Surgical Research, Department of Surgery, Brown University School of Medicine, Providence, Rhode Island 02903

Macrophage (Mphi ) prostaglandin (PG)E2 production has been implicated in immunosuppression and increased susceptibility to sepsis after thermal injury. Deficient interleukin (IL)-12 production has also been implicated in these postburn complications. The present study examined the relationship between Mphi cyclooxygenase (COX)-2 activity and IL-12 production after thermal injury. C57BL/6 female mice were subjected to a 25% total body surface area full-thickness burn. Mphi were isolated 7 days later, or the mice were subjected to sepsis by cecal ligation and puncture (CLP). IL-12 production by Mphi from injured mice was suppressed by >50%, whereas COX-2 expression and PGE2 production were increased twofold. The COX-2 inhibitor NS-398 suppressed PGE2 production and normalized IL-12 production in the injury group, whereas it had no effect on IL-10 production. Injured mice subjected to CLP had lower IL-12 plasma levels compared with sham-treated mice subjected to CLP. NS-398 treatment prevented the suppression in plasma IL-12 levels in the injury group. Thus elevated Mphi COX-2 activity, independent of IL-10, suppresses Mphi IL-12 production after thermal injury and may play an important role in the observed immunosuppression under such conditions.

prostaglandin E2; interleukin-10; immunosuppression; sepsis; burns


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