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Infection-induced airway fibrosis in two rat strains with differential susceptibility
J C McIntosh1, J W Simecka, S E Ross
1Department of Pediatrics, University of Alabama, Birmingham 35233.
Abstract:
Chronic infections play a significant role in the morbidity and mortality of patients with chronic airflow limitation. By stimulating airway inflammation, persistent infection has the potential to cause airway fibrosis. However, in patient this condition is most typically found in lungs damaged by other factors, such as smoking, abnormal secretions, or barotrauma. We report the characterization of Mycoplasma pulmonis infection-induced lung fibrosis in two immunocompetent rat strains with no preexisting lung disease. The fibrosis was predominantly in the airways, as demonstrated by the findings for infected animals of increased airway inflammation, airway fibrosis, and airway wall thickness, which correlated with the collagen content of the lungs. Also, the physiological alterations were the opposite of those found in interstitial fibrosis, with a positive correlation between lung compliance and collagen content. The airway fibrosis was noted earlier and to a greater extent in Lewis rats than in Fisher rats, and this result apparently was related to regulation of the inflammatory response. Airway wall thickness, airway inflammation, and airway fibrosis are commonly reported in tissue specimens from patients with chronic airway diseases and have been shown to correlate with airflow limitation in patients with chronic obstructive pulmonary disease. Thus, this model may be useful in furthering our understanding of the role of chronic infection and airway inflammation in airflow obstruction.
Insights
Chronic Mycoplasma pulmonis infection causes airway fibrosis in rats, offering a new model for studying airflow obstruction. This research highlights the link between persistent infection, airway inflammation, and lung disease progression.
Area of Science:
- Pulmonary Medicine
- Infectious Diseases
- Pathology
Background:
- Chronic infections contribute significantly to morbidity and mortality in chronic airflow limitation.
- Persistent airway infections can lead to airway fibrosis, often in lungs already compromised by other factors.
- Existing models often involve pre-existing lung damage, limiting the study of infection-induced fibrosis.
Purpose of the Study:
- To characterize Mycoplasma pulmonis infection-induced lung fibrosis in immunocompetent rats without prior lung disease.
- To investigate the role of chronic infection and airway inflammation in the development of airway fibrosis and airflow obstruction.
- To establish a novel animal model for studying infection-related pulmonary conditions.
Main Methods:
- Induction of Mycoplasma pulmonis infection in two immunocompetent rat strains (Lewis and Fisher).
- Assessment of airway inflammation, fibrosis, and wall thickness through histological analysis.
- Correlation of fibrotic changes with lung collagen content and physiological parameters like lung compliance.
Main Results:
- Mycoplasma pulmonis infection induced predominantly airway fibrosis, characterized by increased inflammation and wall thickness.
- Fibrotic changes correlated positively with lung collagen content.
- Lewis rats exhibited earlier and more pronounced airway fibrosis compared to Fisher rats, suggesting strain-specific inflammatory responses.
- Physiological alterations observed were distinct from interstitial fibrosis, showing a positive correlation between lung compliance and collagen content.
Conclusions:
- Mycoplasma pulmonis infection is capable of inducing significant airway fibrosis in healthy rats.
- This model provides a valuable tool for understanding the mechanisms linking chronic infection, airway inflammation, and airflow obstruction.
- The findings underscore the importance of addressing chronic infections in the context of chronic airway diseases like COPD.