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Respir Physiol Neurobiol. 2019 Aug;266:9-17. doi: 10.1016/j.resp.2019.04.010. Epub 2019 Apr 22.

Cigarette smoke exposure combined with lipopolysaccharides induced pulmonary fibrosis in mice.

Author information

1
Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
2
Xiangya Nursing School, Central South University, Changsha, Hunan, China.
3
Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China. Electronic address: fengdandan@csu.edu.cn.

Abstract

Cigarette smoke (CS) is a risk factor for pulmonary fibrosis and lipopolysaccharides (LPS) are associated with human occupational lung diseases; however, their combined role in pulmonary fibrosis remains unknown. Therefore, we investigated whether CS combined with LPS induces pulmonary fibrosis in mice. C57BL/6 mice were exposed to CS or normal air for 21 or 35 days, followed by LPS or saline instillation on day 14, 21, and 28. Lung function was tested, and lung tissues were harvested for histological and molecular analyses. Compared to the control, CS and LPS groups, the CS + LPS group showed reduced body weight and survival rate, increased respiratory resistance, decreased lung compliance, marked alveolar structure destruction, and fibrotic lesion formation. Lung tissues showed a considerable increase in IL-6, TNF-α, IL-1β, α-SMA, and TGF-β levels and collagen content. Our results indicate that cigarette smoke exposure followed by LPS in mice induces pulmonary fibrosis with pathophysiology consistent with that of human pulmonary fibrosis.

KEYWORDS:

Cigarette smoke; Collagen deposition; Inflammatory cytokine; Lipopolysaccharide; Pulmonary fibrosis

PMID:
31022471
DOI:
10.1016/j.resp.2019.04.010

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