小鼠肺组织炎症 z-bo 2020-11-25 330

　　Objective: To study the effects of chronic PM2.5 exposure on mouse pneumonia and NLRP3 inflammasome activity, and to provide a new target for the prevention and treatment of PM2.5-induced lung injury.

　　Methods: Male C57BL/6J mice were exposed to PM2.5 by tracheal instillation of different doses, the dose was 2,10mg/(kg∙ bw), and the mice in the control group were instilled with normal saline. Mice were instilled 20 times continuously After exposure every 3 days, blood and lung tissues were taken. Three groups of mice were counted; the levels of macrophages in lung tissues were detected by immunofluorescence staining; the interleukin (IL) in lung tissues was measured with a kit )-1β, IL-18 level and caspase-1 activity; real-time quantitative PCR was used to detect the expression level of NLRP3 inflammasome-related mRNA in lung tissue.

　　Results: Both doses of PM2.5 exposure can significantly reduce the percentage of monocytes (P<0.01), increase the percentage of neutrophils (P<0.01); cause pneumonia; increase lung tissue caspase-1 activity (P <0.01) and the mRNA expression of NLRP3 and ASC (P<0.01). Compared with the control group, the levels of IL-1β and IL-18 in the lung tissue of mice in the two dose groups were significantly increased (P<0.01).

　　Conclusion: Chronic PM2.5 exposure may cause pneumonia by activating the NLRP3 inflammasome of lung tissue.