Abstract: Abstract: Objective To study the role of NLRP3 inflammasome activation of alveolar macrophages in lung injury induced by PM2.5. Methods Rats were made into the lung injury model by intratracheal instillation of high, medium and low doses (15, 10, 5 mg /kg respectively) of PM2.5 suspension collected by medium flow atmospheric sampler. Three days later, the bronchoalveolar lavage was performed, and the phagocytic function of the macrophages in bronchoalveolar lavage fluid (BALF) was measured by neutral red method. And the expression of NLRP3 in lung macrophages was observed by double-immunofluorescent labeling method. The rats were sacrificed, and the lungs were dissected to observe the severity of lung injury by HE staining. The expression of NLRP3 was observed by immunohistochemistry staining. The expressions of IL-18, IL-1β and Caspase-1 in lung tissues were detected by ELISA method. Results By intratracheal instillation of PM2.5, the phagocytic function of macrophages in BALF decreased. And lung injuries of the rats were obvious, manifesting as interstitial pneumonia, significantly widened alveolar septum, partial alveolar wall rupture, especially in the high dose group. The pathological scores of lung tissue were all significantly higher in three experiment groups than those in control group (P＜0. 05). The expressions of NLRP3 in lung tissue were higher in low, medium and high dose groups than those of the control group. The expressions of IL-18, IL-1β and Caspase-1 in lung tissue increased in different degrees. Conclusion The lung injury and inflammatory response caused by PM2.5 are related to the activation of NLRP3 inflammasome in alveolar macrophages in rats.

Key words: dust, air pollutants, macrophages, alveolar, PM2.5, NLRP3 inflammasome