The acute airway inflammation induced by PM exposure and the treatment of essential oils in Balb/c mice.

PM is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM inhalation. Pro-inflammatory cytokine IL-1β generated from effected cells usually plays a crucial role in many kinds of lung inflammatory reactions. The exacerbation of Th immune responses are identified in some PM related diseases. To elucidate the underlying mechanism of PM-induced acute lung inflammation, we exposed Balb/c mice to PM intratracheally and established a mice model. Acute lung inflammation and increased IL-1β expression was observed after PM instillation. Regulatory factors of IL-1β (TLR4/MyD88 signaling pathway and NLRP3 inflammasome) participated in this lung inflammatory response as well. Treatment with compound essential oils (CEOs) substantially attenuated PM-induced acute lung inflammation. The decreased IL-1β and Th immune responses after CEOs treatment were significant. PM may increase the secretion of IL-1β through TLR4/MyD88 and NLRP3 pathway resulting in murine airway inflammation. CEOs could attenuate the lung inflammation by reducing IL-1β and Th immune responses in this model. This study describes a potentially important mechanism of PM-induced acute lung inflammation and that may bring about novel therapies for the inflammatory diseases associated with PM inhalation.