Abstract
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.