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

Martin G Schwacha1, Chun-Shiang Chung, Alfred Ayala

  • 1Center for Surgical Research, Department of Surgery, University of Alabama at Birmingham, 35294, USA. Martin.Schwacha@ccc.uab.edu

American Journal of Physiology. Cell Physiology
|January 15, 2002
PubMed

Insights

Elevated cyclooxygenase-2 (COX-2) activity in macrophages suppresses interleukin-12 (IL-12) production following thermal injury. Inhibiting COX-2 restores IL-12 levels, suggesting a role in post-burn immunosuppression.

Area of Science:

  • Immunology
  • Inflammation Research
  • Burn Injury Complications

Background:

  • Macrophage (Mphi) prostaglandin (PG)E(2) production is linked to immunosuppression and sepsis susceptibility post-thermal injury.
  • Deficient interleukin (IL)-12 production is also implicated in these postburn complications.

Purpose of the Study:

  • To investigate the relationship between Mphi cyclooxygenase (COX)-2 activity and IL-12 production after thermal injury.
  • To determine if COX-2 inhibition can restore IL-12 production and mitigate immunosuppression.

Main Methods:

  • C57BL/6 mice underwent a 25% total body surface area full-thickness burn.
  • Mphi were isolated 7 days post-injury, or mice were subjected to sepsis via cecal ligation and puncture (CLP).
  • Mphi cyclooxygenase (COX)-2 activity and IL-12 production were assessed; COX-2 inhibitor NS-398 was administered.

Main Results:

  • Thermal injury suppressed Mphi IL-12 production by over 50% while increasing COX-2 expression and PGE(2) production twofold.
  • NS-398 treatment suppressed PGE(2) and normalized IL-12 production in injured mice, without affecting IL-10.
  • NS-398 prevented the suppression of plasma IL-12 levels in injured mice subjected to CLP.

Conclusions:

  • Elevated Mphi COX-2 activity, independently of IL-10, suppresses Mphi IL-12 production after thermal injury.
  • This COX-2-mediated suppression of IL-12 may significantly contribute to post-burn immunosuppression and sepsis susceptibility.

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