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Cyclooxygenase-2 suppresses polymorphonuclear neutrophil apoptosis after acute lung injury

Zhang Jinzhou1, He Tao, Chen Wensheng

  • 1Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an, People's Republic of China.

The Journal of Trauma
|April 12, 2008
PubMed
Abstract

Insights

Increased cyclo-oxygenase-2 (COX-2) expression suppresses polymorphonuclear neutrophil (PMN) apoptosis following acute lung injury (ALI). Targeting COX-2 may offer a novel therapeutic strategy for ALI by promoting PMN cell death.

Area of Science:

  • Immunology
  • Cell Biology
  • Pulmonary Medicine

Background:

  • Polymorphonuclear neutrophil (PMN) apoptosis is suppressed in acute lung injury (ALI), hindering resolution.
  • Mechanisms of PMN apoptosis suppression in ALI remain unclear.
  • Cyclo-oxygenase-2 (COX-2) is upregulated by inflammatory mediators in PMNs and regulates apoptosis in other cell types.

Purpose of the Study:

  • To investigate the role of cyclo-oxygenase-2 (COX-2) expression in suppressing PMN apoptosis after acute lung injury (ALI).

Main Methods:

  • Acute lung injury (ALI) was induced in rabbits; COX-2 expression and PMN apoptosis in bronchoalveolar lavage fluid (BALF) were analyzed.
  • In vitro, normal PMNs were treated with BALF from injured lungs (BALFALI) with or without a COX-2 inhibitor (NS398).
  • Apoptosis was measured by flow cytometry; COX-2 mRNA levels were assessed.

Main Results:

  • PMN apoptosis was decreased, while COX-2 expression was increased in BALF after ALI.
  • A significant inverse correlation was observed between COX-2 protein expression and PMN apoptosis (gamma = -0.75, p < 0.01).
  • BALFALI reduced PMN apoptosis and increased COX-2 mRNA in vitro; NS398 partially reversed these effects.

Conclusions:

  • Upregulation of intrapulmonary COX-2 expression contributes to the suppression of PMN apoptosis in ALI.
  • Targeting COX-2 may represent a therapeutic strategy for ALI.

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