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Published on: October 19, 2013

Cyclooxygenase-2 in newborn hyperoxic lung injury

Rodney D Britt1, Markus Velten2, Trent E Tipple3

  • 1Center for Perinatal Research, The Research Institute at Nationwide Children's Hospital, 700 Children's Drive, Columbus, OH 43205, USA.

Free Radical Biology & Medicine
|April 30, 2013
PubMed

Insights

Cyclooxygenase-2 (COX-2) inhibition reduced inflammation in newborn mice exposed to high oxygen, but did not prevent lung developmental deficits associated with bronchopulmonary dysplasia (BPD). This suggests COX-2 may be a therapeutic target for BPD-related inflammation.

Area of Science:

  • Neonatal physiology
  • Pulmonary medicine
  • Inflammation research

Background:

  • Bronchopulmonary dysplasia (BPD) is a chronic lung disease in preterm infants, often caused by supraphysiological oxygen concentrations and mechanical ventilation.
  • Hyperoxia exposure in newborn mice mimics BPD, leading to inflammation and impaired alveolarization.
  • Pulmonary cyclooxygenase-2 (COX-2) expression is elevated in hyperoxia-exposed newborn mice.

Purpose of the Study:

  • To investigate the role of COX-2 in hyperoxia-induced lung injury in newborn mice.
  • To test the hypothesis that inhibiting COX-2 activity would reduce inflammation and improve alveolarization.

Main Methods:

  • Newborn mice were treated with vehicle, aspirin, or celecoxib (COX-2 inhibitors) or used as wild-type, heterozygous, or homozygous COX-2 knockout models.
  • Mice were exposed to room air or 85% oxygen for 14 days.
  • Inflammatory markers, including monocyte chemoattractant protein-1 (MCP-1) and macrophage counts, were assessed in bronchoalveolar lavage fluid and lung tissue.

Main Results:

  • Aspirin and COX-2 knockout mice showed reduced MCP-1 levels in bronchoalveolar lavage fluid.
  • Aspirin and celecoxib treatments decreased macrophage infiltration and attenuated hyperoxia-induced COX activity.
  • Despite reduced inflammation, COX-2 inhibition did not prevent hyperoxia-induced lung developmental deficits.

Conclusions:

  • Increased COX-2 activity contributes to inflammatory responses, such as macrophage chemotaxis, during hyperoxia exposure.
  • Modulating COX-2 activity may be a potential therapeutic strategy to mitigate hyperoxia-induced inflammation in preterm infants at risk for BPD.
  • COX-2 inhibition alone does not fully prevent the lung structural damage associated with hyperoxia.

Keywords:
Bronchopulmonary dysplasiaCyclooxygenase-2HyperoxiaProstaglandins

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