Antagonism of interleukin 17 protects chronic obstructive pulmonary disease rat lungs from adverse effects of environmental PM2.5.

Severe air pollution has raised concerns about the adverse effects of particulate matters 2.5 μm in size (PM2.5) on human health. However, the mechanisms elucidating how PM2.5 affects lungs, especially in COPD, remain unclear. In this study, we examined the concentration changes of environmental PM2.5 from 2013 to 2019 in Shijiazhuang city. PM2.5 was collected to study its effects on a COPD lung. Inflammatory factors present in bronchoalveolar lavage fluid (BLF) were examined after exposure. An antagonist of IL-17 was used to reverse PM2.5-induced pathological and functional impairments in COPD rat lungs. Our results show that the degree of air pollution changed significantly (55.873, P < 0.001) during the study period in accordance with PM tendency. PM2.5 and PM10 was present in higher concentrations from December 2013 to January 2014 and December 2016 to January 2017, respectively. After COPD rats were exposed to PM2.5 for 2 or 4 weeks, all indicators of lung function (FEV0.3, FVC, FEV0.3/FVC, PEF, Rrs) decreased continuously and significantly. The levels of TGF-β1, IL-6, IL-17, and IL-21 in BLF, as well as the expression of IL-17 in lung tissues, were significantly increased after exposure for 2 or 4 weeks. When an IL-17 antagonist was introduced following PM2.5 exposure, inflammatory factor levels in BLF and pathological scores of lung tissues decreased significantly. Moreover, lung functions were partially rescued. Collectively, our data demonstrate that IL-17 is a potential therapeutic target for COPD lungs after PM2.5 exposure.