Air Pollution Section
Particulate matter disrupts airway epithelial barrier via oxidative stress to promote Pseudomonas aeruginosa infection
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.
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.
