Jinguo Liu1, Xiaoyan Chen1, Maosen Dou2, Hong He3,4, Mohan Ju1, Shimeng Ji1, Jian Zhou1, Cuicui Chen1, Donghui Zhang1, Changhong Miao3,4, Yuanlin Song1,5,6. 1. Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University and Shanghai Respiratory Research Institute, Shanghai 200032, China. 2. Department of Infectious Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China. 3. Department of Anesthesiology, Fudan University Shanghai Cancer Center, Shanghai 200032, China. 4. Department of Oncology, Shanghai Medical College, Fudan University, Shanghai 200032, China. 5. Department of Respiratory Medicine, Shanghai Public Health Clinical Center, Fudan University, Shanghai 200032, China. 6. Department of Pulmonary Medicine, Zhongshan Hospital, Qingpu Branch, Shanghai 200032, China.
Abstract
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: In vitro, 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. In vivo, 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.
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: In vitro, 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. In vivo, 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.
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