Glucocorticoid enhances viability of human respiratory epithelial cells inflicted by ambient particulate matter

Particulate matter (PM) is one of the most common ambient air pollutants, which is derived from diesel engines, wildfires, yellow dust, and other combustion sources. Especially, PM with an aerodynamic diameter of <2.5 μm (PM2.5) enhances risks of damaging respiratory organs. Previous studies have reported that PMinduced autophagy and apoptosis can be considered as a phenomenal molecular mechanism of PM-mediated cytotoxicity in lung cancer epithelial cells. In this study, we investigate the effects of PM2.5 on cellular responses in human nasal epithelial primary cells and lung cancer cells. The respiratory epithelial cells showed both time- and concentration-dependent decrease of cell viability when the cells were exposed to PM, which can be attributed to increased levels of reactive oxygen species (ROS) in the cells. In addition to inducing autophagy via increase of microtubule-associated protein light chain-3 (LC3) puncta, PMexposure also induced the expression of inflammatory cytokines such as IL-6 and 8 in human respiratory epithelial cells. Thus, inflammation response, as well as autophagosome formation due to increased ROS, is responsible for apoptotic death of respiratory epithelial cells under challenge of PM. The glucocorticoid ciclesonide used to treat asthma and allergic rhinitis was shown to be effective in reducing cellular mortality, probably by reducing inflammatory cytokines. These results suggest that PM2.5-induced inflammation plays a key role in apoptotic cell death in respiratory epithelial cells, which may be treated by an anti-inflammatory glucocorticoid.