Abstract
Polluting particulate matter suspended in the air is a leading cause of lung carcinogenesis, a process often accompanied by epithelial to mesenchymal transition (EMT) of the bronchial epithelium. By providing a continuous supply of nutrients, microfluidic chips simulate the spatial characteristics of the cellular environment to enable integrated, flexible and high-throughput analysis of cell growth and function. Here, we used a microfluidic chip to evaluate the effects of the air pollutant PM2.5 on EMT in human bronchial epithelial 16HBE cells and on alveolar macrophage chemotaxis. PM2.5 induced NF-κB, PI3K, Snail and N-cadherin levels and repressed E-cadherin levels in 16HBE cells and promoted macrophage chemotaxis. Collectively, our results indicate that PM2.5 causes EMT in bronchial epithelial cells via induction of inflammatory pathways and shed light upon its pathological effects in humans.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
