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