Autophagy inhibitors suppress environmental particulate matter-induced airway inflammation

- PM induced autophagy in HBE cells and in mouse airway epithelium.
- Autophagy inhibitors suppressed PM-induced airway inflammation in vitro and in vivo.
- Autophagy inhibitors suppressed PM-induced inflammation response through NF-κB pathway.

Particulate matter (PM) is a significant risk factor for airway injury. We have recently demonstrated a pivotal role of autophagy in mediating PM-induced airway injury. In the present study, we examined the possible effects of autophagy inhibitors spautin-1 and 3-Methyladenine (3-MA) in protection of PM-induced inflammatory responses. We observed that PM triggered autophagy in human bronchial epithelial (HBE) cells and in mouse airways. Spautin-1 or 3-MA inhibited PM-induced expression of inflammatory cytokines in HBE cells, and decreased the neutrophil influx and proinflammatory cytokines induced by PM in vivo. We further illustrated that autophagy inhibitors suppressed the inflammation responses via inhibition of the nuclear factor-кB (NF-кB) pathway. Thus, this study shows a paradigm that autophagy inhibitors effectively decrease the PM-induced airway inflammation via suppressing the NF-кB pathway, which may provide novel preventive and/or protective approaches for PM-related airway injury.