Department of Physiology, Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Xiangya Nursing School, Central South University, Changsha, Hunan, China.
Respir Physiol Neurobiol. 2019 Aug;266:9-17. doi: 10.1016/j.resp.2019.04.010. Epub 2019 Apr 22.
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.
香烟烟雾（CS）是肺纤维化的一个风险因素，脂多糖（LPS）与人类职业性肺病有关；然而，它们在肺纤维化中的共同作用尚不清楚。因此，我们研究了 CS 与 LPS 联合是否会在小鼠中诱导肺纤维化。C57BL/6 小鼠暴露于 CS 或正常空气中 21 或 35 天，然后在第 14、21 和 28 天进行 LPS 或盐水滴注。测试肺功能，并采集肺组织进行组织学和分子分析。与对照组相比，CS 和 LPS 组，CS+LPS 组表现出体重减轻和存活率降低、呼吸阻力增加、肺顺应性降低、肺泡结构破坏和纤维性病变形成。肺组织中 IL-6、TNF-α、IL-1β、α-SMA 和 TGF-β 水平以及胶原含量明显增加。我们的结果表明，香烟烟雾暴露后再用 LPS 处理小鼠可诱导肺纤维化，其病理生理学与人类肺纤维化一致。
