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Abstract Title:

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

Abstract Source:

Respir Physiol Neurobiol. 2019 Aug ;266:9-17. Epub 2019 Apr 22. PMID: 31022471

Abstract Author(s):

Lijuan Fang, Qingmei Cheng, Feiyan Zhao, Haipeng Cheng, Yongyu Luo, Xingwen Bao, Yanghang Li, Xinyue Liang, Yanhong Huang, Jianping Xu, Jianzhong Han, Yiting Tang, Siyuan Tang, Wei Liu, Ziqiang Luo, DanDan Feng

Article Affiliation:

Lijuan Fang

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.

Study Type : Animal Study

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