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

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

Research output: Contribution to journalArticlepeer-review

40 Scopus citations

Abstract

Macrophage (Mφ) 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 Mφ 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. Mφ were isolated 7 days later, or the mice were subjected to sepsis by cecal ligation and puncture (CLP). IL-12 production by Mφ 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 Mφ COX-2 activity, independent of IL-10, suppresses Mφ IL-12 production after thermal injury and may play an important role in the observed immunosuppression under such conditions.

Original languageEnglish (US)
Pages (from-to)C263-C270
JournalAmerican Journal of Physiology - Cell Physiology
Volume282
Issue number2 51-2
DOIs
StatePublished - 2002

Keywords

  • Burns
  • Immunosuppression
  • Interleukin-10
  • Prostaglandin E
  • Sepsis

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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