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. 2020 Sep 15;12(9):5808-5817.
eCollection 2020.

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

Haitao Li  1 , Xixin Yan  1 , Shan Feng  1 , Shuai Li  1 , Huiran Zhang  1 , Jingwen Li  1 , Tianjie Qi  1
Affiliations

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

Haitao Li et al. Am J Transl Res. .

Abstract

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.

Keywords: COPD model; Environmental PM2.5; IL-17 antibody; inflammatory factors; lung impairment.

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Conflict of interest statement

None.

Figures

Figure 1
Figure 1
The concentrations of PM2.5 and PM10 in winter (December to January) from 2013 to 2019. A. The concentration of PM2.5. B. The concentration of PM10. All data are represented in a box plot, and were examined by the independent-sample Kruskai-Wallis H test.
Figure 2
Figure 2
IL-17 expression levels were examined by western blot analysis of COPD rats exposed to PM2.5 for 2 or 4 weeks. Differences between the three groups were compared after densitometry and quantitation using Image J software for three independent experiments. The data were analyzed by ANOVA. GAPDH was used as a loading control and the data are presented as the mean ± SD. **P < 0.01.
Figure 3
Figure 3
Lung tissues were examined by hematoxylin-eosin (HE) staining after COPD modeling, PM2.5 exposure, and IL-17 antibody treatment. Neutrophil infiltration, ciliated columnar epithelium, alveolar septa, alveolar cavity, and alveolar walls were observed by light microscopy. A. Healthy lungs. B. Rat lungs after COPD modeling. C. Rat lungs exposed to PM2.5 for 2 weeks after COPD modeling. D. Effect of IL-17 antibody injection after COPD rats were exposed to PM2.5 for 2 weeks. E. Rat lungs exposed to PM2.5 for 4 weeks after COPD modeling. F. Effect of IL-17 antibody injection after COPD rats were exposed to PM2.5 for 4 weeks.
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References

    1. Song C, Wu L, Xie Y, He J, Chen X, Wang T, Lin Y, Jin T, Wang A, Liu Y, Dai Q, Liu B, Wang YN, Mao H. Air pollution in China: status and spatiotemporal variations. Environ Pollut. 2017;227:334–347. - PubMed
    1. Qiao B, Chen Y, Tian M, Wang H, Yang F, Shi G, Zhang L, Peng C, Luo Q, Ding S. Characterization of water soluble inorganic ions and their evolution processes during PM2.5 pollution episodes in a small city in southwest China. Sci Total Environ. 2019;650:2605–2613. - PubMed
    1. Bergstra AD, Brunekreef B, Burdorf A. The mediating role of risk perception in the association between industry-related air pollution and health. PLoS One. 2018;13:e0196783. - PMC - PubMed
    1. Hammond D, Croghan C, Shin H, Burnett R, Bard R, Brook RD, Williams R. Cardiovascular impacts and micro-environmental exposure factors associated with continuous personal PM2.5 monitoring. J Expo Sci Environ Epidemiol. 2014;24:337–345. - PubMed
    1. Ma QY, Huang DY, Zhang HJ, Wang S, Chen XF. Exposure to particulate matter 2.5 (PM2.5) induced macrophage-dependent inflammation, characterized by increased Th1/Th17 cytokine secretion and cytotoxicity. Int Immunopharmacol. 2017;50:139–145. - PubMed

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