颗粒物通过氧化应激破坏气道上皮屏障，从而促进感染。
Particulate matter disrupts airway epithelial barrier via oxidative stress to promote infection.
作者信息
Liu Jinguo, Chen Xiaoyan, Dou Maosen, He Hong, Ju Mohan, Ji Shimeng, Zhou Jian, Chen Cuicui, Zhang Donghui, Miao Changhong, Song Yuanlin
机构信息
Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, Shanghai 200032, China.
Department of Infectious Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
出版信息
J Thorac Dis. 2019 Jun;11(6):2617-2627. doi: 10.21037/jtd.2019.05.77.
BACKGROUND
Airborne particulate matter (PM) is associated with increasing susceptibility to respiratory bacterial infection. Tight junctions (TJs) are protein complexes that form airway epithelial barrier against infection. This study aimed to investigate the effects of PM on the airway TJs in response to infection.
METHODS
The cytotoxicity of PM to BEAS-2B was evaluated. The reactive oxygen species (ROS) production was measured by the flow cytometry. Colony forming units (CFUs) assay and confocal microscopy were utilized to evaluate the number of bacteria. Immunofluorescence and western blot assay were conducted to detect the expressions of TJs proteins. Animal models were used to investigate the role of TJs in PM-induced lung injury upon bacterial infection.
RESULTS
, PM decreased cell viability, increased ROS production, and increased the number of intracellular bacteria accompanying by the degradation of TJs. N-acetylcysteine (NAC) significantly reversed the PM-induced bacterial invasion and PM-induced disruption of TJs. , PM increases bacteria-infected lung injury, lung bacteria burden and blood bacterial dissemination, which was closely correlated to the degradation of TJs.
CONCLUSIONS
PM disrupts TJs via oxidative stress to promote bacterial infection.
背景
空气中的颗粒物（PM）与呼吸道细菌感染易感性增加有关。紧密连接（TJs）是形成气道上皮屏障以抵御感染的蛋白质复合物。本研究旨在探讨PM对感染时气道TJs的影响。
方法
评估PM对BEAS-2B的细胞毒性。通过流式细胞术测量活性氧（ROS）的产生。采用菌落形成单位（CFUs）测定和共聚焦显微镜评估细菌数量。进行免疫荧光和蛋白质印迹分析以检测TJs蛋白的表达。使用动物模型研究TJs在细菌感染时PM诱导的肺损伤中的作用。
结果
PM降低细胞活力，增加ROS产生，并伴随TJs降解增加细胞内细菌数量。N-乙酰半胱氨酸（NAC）显著逆转PM诱导的细菌侵袭和PM诱导的TJs破坏。PM增加细菌感染的肺损伤、肺细菌负荷和血液细菌播散，这与TJs降解密切相关。
结论
PM通过氧化应激破坏TJs以促进细菌感染。
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