Biomass-related PM2.5 induced inflammatory microenvironment via IL-17F/IL-17RC axis

Fang He; Xiaoyuan Yu; Jiahuan Zhang; Jieda Cui; Lei Tang; Siqi Zou; Jinding Pu; Pixin Ran

doi:10.1016/j.envpol.2023.123048

Biomass-related PM_2.5 induced inflammatory microenvironment via IL-17F/IL-17RC axis

Environ Pollut. 2024 Feb 1:342:123048. doi: 10.1016/j.envpol.2023.123048. Epub 2023 Nov 28.

Authors

Fang He¹, Xiaoyuan Yu², Jiahuan Zhang³, Jieda Cui⁴, Lei Tang², Siqi Zou², Jinding Pu⁵, Pixin Ran⁶

Affiliations

¹ School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 510000, China; State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510000, China.
² School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, Guangdong, 510000, China.
³ State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510000, China.
⁴ State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510000, China; Guangzhou National Laboratory, No.9 XingDaoHuanBei Road, Guangzhou International BioIsland, Guangzhou, Guangdong, 510000, China.
⁵ Department of Pulmonary and Critical Care Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510000, China.
⁶ State Key Laboratory of Respiratory Diseases, National Clinical Research Center for Respiratory Diseases, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, 510000, China; Guangzhou National Laboratory, No.9 XingDaoHuanBei Road, Guangzhou International BioIsland, Guangzhou, Guangdong, 510000, China. Electronic address: pxran@gzhmu.edu.cn.

PMID: 38036089
DOI: 10.1016/j.envpol.2023.123048

Abstract

Biomass exposure is a significant environmental risk factor for COPD, but the underlying mechanisms have not yet been fully elucidated. Inflammatory microenvironment has been shown to drive the development of many chronic diseases. Pollution exposure can cause increased levels of inflammatory factors in the lungs, leading to an inflammatory microenvironment which is prevalent in COPD. Our findings revealed that IL-17F was elevated in COPD, while exposure to biomass led to increased expression of IL-17F in both alveolar epithelial and macrophage cells in mice. Blocking IL-17F could alleviate the lung inflammation induced by seven days of biomass exposure in mice. We employed a transwell co-culture system to simulate the microenvironment and investigate the interactions between MLE-12 and MH-S cells. We demonstrated that anti-IL-17F antibody attenuated the inflammatory responses induced by BRPM_2.5 in MLE-12 and MH-S co-cultured with BRPM_2.5-MLE-12, which reduced inflammatory changes in microenvironment. We found that IL-17RC, an important receptor for IL-17F, played a key role in the interactions. Knockout of IL-17RC in MH-S resulted in inhibited IL-17F signaling and attenuated inflammatory response after MH-S co-culture with BRPM_2.5-MLE-12. Our investigation suggests that BRPM_2.5 induces lung epithelial-macrophage interactions via IL-17F/IL-17RC axis regulating the inflammatory response. These results may provide a novel strategy for effective prevention and treatment of biomass-related COPD.

Keywords: Biomass-related PM; COPD; IL-17F; IL-17RC; Inflammatory microenvironment.

MeSH terms

Animals
Biomass
Interleukin-17*
Mice
Mice, Knockout
Particulate Matter / toxicity
Pulmonary Disease, Chronic Obstructive*
Receptors, Interleukin-17 / metabolism

Substances

Interleukin-17
Receptors, Interleukin-17
Particulate Matter