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Updated: Jul 15, 2026
06:03
Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
Published on: May 9, 2025
Cyclooxygenase-2 deficiency exacerbates bleomycin-induced lung dysfunction but not fibrosis
Jeffrey W Card1, James W Voltz, Michelle A Carey
1Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, NC 27709, USA.
Summary
Cyclooxygenase-2 (COX-2) deficiency did not affect lung fibrosis severity in mice. However, COX-2 plays a key role in maintaining lung function during pulmonary fibrosis, a role that can be modulated by COX-1.
Area of Science:
- Pulmonary medicine
- Immunology
- Molecular biology
Background:
- Cyclooxygenase (COX)-derived eicosanoids are implicated in pulmonary fibrosis pathogenesis.
- The specific role of COX-2 in experimental pulmonary fibrosis remains unclear.
Purpose of the Study:
- To investigate the fibrotic and functional effects of bleomycin in COX-2 deficient mice.
- To assess the impact of airway-specific COX-1 overexpression on fibrotic and functional outcomes in wild-type and COX-2 knockout mice.
Main Methods:
- Intratracheal bleomycin administration in wild-type and COX-2 knockout mice.
- Assessment of airway cell influx, lung collagen content, and respiratory mechanics.
- Evaluation of airway-specific COX-1 overexpression effects.
Main Results:
- COX-2 deficiency did not alter bleomycin-induced lung fibrosis severity.
- Bleomycin caused more severe respiratory mechanics impairment in COX-2 knockout mice.
- COX-1 overexpression prevented lung function decline in bleomycin-treated COX-2 knockout mice, correlating with reduced cysteinyl leukotriene levels.
Conclusions:
- COX-2 is crucial for maintaining lung function during pulmonary fibrosis, not for fibrosis progression itself.
- COX-1 can modulate lung function deficits in the context of pulmonary fibrosis and COX-2 deficiency.
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