Microfluidic analysis of PM2.5-induced epithelial–mesenchymal transition in human bronchial epithelial 16HBE cells

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.