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pubmed-article:11788337pubmed:abstractTextMacrophage (Mphi) prostaglandin (PG)E(2) 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 PGE(2) production were increased twofold. The COX-2 inhibitor NS-398 suppressed PGE(2) 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.lld:pubmed
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pubmed-article:11788337pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:11788337pubmed:articleTitleCyclooxygenase 2-mediated suppression of macrophage interleukin-12 production after thermal injury.lld:pubmed
pubmed-article:11788337pubmed:affiliationCenter for Surgical Research, Department of Surgery, University of Alabama at Birmingham, 35294, USA. Martin.Schwacha@ccc.uab.edulld:pubmed
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pubmed-article:11788337pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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