Macrophage STING signaling promotes fibrosis in benign airway stenosis via an IL6-STAT3 pathway

YiLin Chen, ChengCheng Yang, YuShan Miao, DongChen Shi, Xiang Li, Sen Tian, YiFei Zhang, ChengFei Xu, YuChao Dong, ChaoFeng Han (), Hui Shi () and Chong Bai ()
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YiLin Chen: The First Affiliated Hospital of Naval Medical University
ChengCheng Yang: The First Affiliated Hospital of Naval Medical University
YuShan Miao: The First Affiliated Hospital of Naval Medical University
DongChen Shi: The First Affiliated Hospital of Naval Medical University
Xiang Li: General Hospital of Central Theater Command of Chinese People’s Liberation Army
Sen Tian: No. 906 Hospital of the Chinese People’s Liberation Army Joint Logistic Support Force
YiFei Zhang: The First Affiliated Hospital of Naval Medical University
ChengFei Xu: The First Affiliated Hospital of Naval Medical University
YuChao Dong: The First Affiliated Hospital of Naval Medical University
ChaoFeng Han: Naval Medical University
Hui Shi: The First Affiliated Hospital of Naval Medical University
Chong Bai: The First Affiliated Hospital of Naval Medical University

Nature Communications, 2025, vol. 16, issue 1, 1-20

Abstract: Abstract Acute and chronic inflammation are important pathologies of benign airway stenosis (BAS) fibrosis, which is a frequent complication of critically ill patients. cGAS-STING signalling has an important role in inflammation and fibrosis, yet the function of STING in BAS remains unclear. Here we demonstrate using scRNA sequencing that cGAS‒STING signalling is involved in BAS, which is accompanied by increased dsDNA, expression and activation of STING. STING inhibition or deficiency effectively alleviates tracheal fibrosis of BAS mice by decreasing both acute and chronic inflammation. Macrophage depletion also effectively ameliorates BAS. Mechanistically, dsDNA from damaged epithelial cells activates the cGAS-STING pathway of macrophages and induces IL-6 to activate STAT3 and promote fibrosis. In summary, the present results suggest that cGAS-STING signalling induces acute inflammation and amplifies the chronic inflammation and tracheal fibrosis associated with benign airway stenosis, highlighting the mechanism and potential drug target of BAS.

Date: 2025
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DOI: 10.1038/s41467-024-55170-5

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