[Exposure of acute severe air pollution promotes inflammatory cell infiltration and increases the levels of proinflammatory cytokines and chemokines in lung tissues of rats].

Objective To observe the effect of acute severe air pollution exposure on cytokines and chemokines in lung tissues of rats and explore its significance. Methods During the period of severe air pollution in Beijing from December 17 to 22, 2016, rats were exposed to air pollution for 6 days, and then sacrificed on the 7th day. Lung tissues were taken and their histological changes were observed by HE staining. The levels of 22 cytokines/chemokines in the lung tissue homogenate supernatant were detected by liquid chip method. Results Compared with the control group, the lung tissues of the rats in the air pollution exposure group were characterized by widened alveolar septum, inflammatory cell infiltration and vascular bleeding. Chemokines eotaxin, monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-2 (MIP-2), regulated on activation, normal T cell expressed and secreted factor (RANTES), and proinflammatory cytokines interleukin 1β (IL-1β), IL-17, IL-18, tumor necrosis factor α (TNF-α) in the supernatant of lung homogenate of rats in the air pollution exposure group significantly increased. But anti-inflammatory IL-10 significantly decreased. Th1 cytokines IL-2 and interferon-γ (IFN-γ) did not change, and Th2 cytokines IL-5 increased by 1.65 times and IL-10 decreased by 0.82 times. Conclusion Acute severe air pollution exposure can lead to inflammatory response in lung tissues of rats. The secretion of chemokines eotaxin, MCP-1, MIP-2, RANTES and proinflammatory cytokines IL-1β, IL-17, IL-18, TNF-α are promoted in this process. The infiltrated T cells in lung tissues are dominated by Th2 cells.