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PM 2.5  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 2.5  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 2.5  related diseases. To elucidate the underlying mechanism of PM 2.5 -induced acute lung inflammation, we exposed Balb/c mice to PM 2.5  intratracheally and established a mice model. Acute lung inflammation and increased IL-1β expression was observed after PM 2.5  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 2.5 -induced acute lung inflammation. The decreased IL-1β and Th immune responses after CEOs treatment were significant. PM 2.5  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 2.5 -induced acute lung inflammation and that may bring about novel therapies for the inflammatory diseases associated with PM 2.5  inhalation.

The acute airway inflammation induced by PM2.5 exposure and the treatment of essential oils in Balb/c mice