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Updated: Oct 3, 2026

Pseudomonas aeruginosa Induced Lung Injury Model
Published on: October 29, 2014
Pseudomonas aeruginosa-induced lung injury: role of oxidative stress
Zacharias E Suntres1, Abdelwahab Omri, Pang N Shek
1Biomedical Sciences Section, Defence and Civil Institute of Environmental Medicine, Toronto, Ontario, Ontario M3M 3B9, Canada. Zach.Suntres@dciem.dnd.ca
Abstract:
Pseudomonas aeruginosa is a Gram-negative pathogen that can cause lung injury in immunocompromised patients, primarily by inducing a release of host-derived mediators responsible for the influx of phagocytes to the lung. These phagocytes exert their antimicrobial actions by releasing toxic metabolites, including reactive oxygen species and proteases, which can also cause cell injury. This study was carried out to assess the pulmonary oxidant-antioxidant status of male adult Sprague-Dawley rats infected with different numbers of P. aeruginosa (10(4)-10(7)cfu/animal). Intratracheal instillation of P. aeruginosa resulted in lung injury, as evidenced by increases in wet lung weight and decreases in the lung activities of angiotensin converting enzyme and alkaline phosphatase, enzymes localized primarily in pulmonary endothelial and alveolar type II epithelial cells, respectively. The P. aeruginosa -induced lung injury was directly related to the infiltration of neutrophils, as indicated by increases in myeloperoxidase activity. The challenge of animals with P. aeruginosa resulted in increases in lipid peroxidation and decreases in glutathione content, which were associated with the indices of lung injury and neutrophil infiltration. Such a challenge also resulted in weakening the antioxidant defence system, as evidenced by decreases in superoxide dismutase, catalase and glutathione peroxidase activities. These data suggest that changes in the pulmonary oxidant-antioxidant status may play an important role in the P. aeruginosa -induced lung injury.
Insights
Pseudomonas aeruginosa infection causes lung injury by increasing oxidative stress and weakening the lung
Area of Science:
- Pulmonary Medicine
- Microbiology
- Toxicology
Background:
- Pseudomonas aeruginosa is a Gram-negative pathogen that causes lung injury, particularly in immunocompromised individuals.
- Phagocyte influx into the lungs, induced by P. aeruginosa, releases toxic metabolites, leading to cell injury.
- Oxidative stress and antioxidant imbalance are implicated in pathogen-induced lung damage.
Purpose of the Study:
- To investigate the pulmonary oxidant-antioxidant status in Sprague-Dawley rats following infection with P. aeruginosa.
- To correlate changes in oxidant-antioxidant markers with the severity of lung injury and neutrophil infiltration.
Main Methods:
- Male adult Sprague-Dawley rats were intratracheally instilled with varying concentrations of P. aeruginosa (10^4–10^7 cfu/animal).
- Lung injury was assessed by measuring lung weight and the activity of angiotensin converting enzyme and alkaline phosphatase.
- Neutrophil infiltration was quantified using myeloperoxidase activity.
- Oxidant markers (lipid peroxidation) and antioxidant markers (glutathione, superoxide dismutase, catalase, glutathione peroxidase) were measured.
Main Results:
- P. aeruginosa infection led to significant lung injury, indicated by increased lung weight and decreased enzyme activities.
- Neutrophil infiltration, measured by myeloperoxidase activity, correlated directly with the extent of lung injury.
- Infection resulted in increased lipid peroxidation and decreased glutathione levels, signifying oxidative stress.
- Activities of key antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase) were significantly reduced.
Conclusions:
- P. aeruginosa infection induces significant lung injury in rats, characterized by oxidative stress and impaired antioxidant defenses.
- The observed changes in pulmonary oxidant-antioxidant balance are closely linked to neutrophil infiltration and lung damage.
- These findings highlight the critical role of oxidative-antioxidative status in the pathogenesis of P. aeruginosa-induced lung injury.
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