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Published on: January 16, 2015
Altered expression of antimicrobial molecules in cigarette smoke-exposed emphysematous mice lungs
Yoko Shibata1, Shuichi Abe, Sumito Inoue
1Department of Cardiology, Yamagata University School of Medicine, Yamagata, Japan. shibata@med.id.yamagata-u.ac.jp
Background And Objective:
The natural history of COPD, a disease usually caused by cigarette smoking, is associated with frequent respiratory infections. Consistent with human COPD, bacterial clearance in the lungs has been reported to be impaired in mice exposed to cigarette smoke. In the airways, several antimicrobial molecules such as surfactant proteins (SP), beta-defensins (BD), secretory leucocyte protease inhibitor (SLPI) and lysozyme play important roles in the defence against invading pathogens. This study evaluated the expression of antimicrobial molecules in mice lungs with cigarette smoke-induced emphysematous changes.
Methods:
Six B6C3F1 mice were exposed to cigarette smoke (2 cigarettes/day/mouse for 6 months) or room air. Gene expression within the lungs of mice in both groups was assessed by RT-PCR.
Results:
The expression of SP-A, BD2, BD3 and SLPI was significantly elevated in the lungs of cigarette smoke-exposed mice compared with air-exposed mice. BD1 expression decreased in the smoke-exposed mice and lysozyme expression was unchanged.
Conclusions:
Chronic cigarette smoke exposure did not suppress the expression of antimicrobial molecules in the lung. Altered expression of antimicrobial molecules in this mouse model does not explain the impaired host defence against respiratory microbes seen in patients with COPD.
Insights
Chronic cigarette smoke exposure in mice increased some antimicrobial molecules like surfactant proteins (SP) and beta-defensins (BD) but did not explain impaired lung defense in COPD.
Area of Science:
- Pulmonary Medicine
- Immunology
- Toxicology
Background:
- Chronic Obstructive Pulmonary Disease (COPD) is linked to frequent respiratory infections, potentially due to impaired bacterial clearance.
- Cigarette smoke exposure in mice mimics some aspects of human COPD, including compromised lung defense mechanisms.
- Antimicrobial molecules such as surfactant proteins (SP), beta-defensins (BD), secretory leucocyte protease inhibitor (SLPI), and lysozyme are crucial for lung defense against pathogens.
Purpose of the Study:
- To investigate the expression of key antimicrobial molecules in mouse lungs following chronic cigarette smoke exposure.
- To determine if cigarette smoke exposure alters the expression of pulmonary antimicrobial molecules relevant to host defense.
Main Methods:
- Mice were exposed to cigarette smoke or room air for six months.
- Gene expression of antimicrobial molecules in lung tissue was quantified using RT-PCR.
Main Results:
- Expression of surfactant protein A (SP-A), beta-defensin 2 (BD2), beta-defensin 3 (BD3), and SLPI was significantly upregulated in smoke-exposed mice.
- Beta-defensin 1 (BD1) expression was decreased, while lysozyme expression remained unchanged in the lungs of mice exposed to cigarette smoke.
Conclusions:
- Chronic cigarette smoke exposure does not suppress the overall expression of antimicrobial molecules in the mouse lung.
- The observed alterations in antimicrobial molecule expression in this model do not account for the impaired host defense against respiratory microbes seen in COPD patients.
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