Macrophage STING signaling promotes fibrosis in benign airway stenosis via an IL6-STAT3 pathway
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Abstract
Abstract Benign airway stenosis (BAS) caused by tracheal intubation resuscitation measures is a difficult complication to ignore in the management of critically ill patients. However, the pathogenesis of this disease, which is characterized histologically by tracheal fibrosis, remains poorly understood. It has been shown that post-injury inflammatory processes play a key role in tissue fibrosis. However, we remain unclear about the relationship between inflammation induced by mechanical injury and BAS after tracheal intubation. Here, we found STING expression was increased in trachea after injury and inhibition or deletion of STING can alleviate tracheal fibrosis in BAS mice. Then, we reveal that released tracheal epithelial cell DNA resulting from mechanical injury activates macrophage STING. Further, macrophages with activated cGAS-STING pathway promote fibroblast fibrosis in the trachea via the IL6-STAT3 axis. We determined that the cGAS-STING pathway in macrophages is critical in causing tracheal fibrosis and ultimately benign airway stenosis. Our results provide a key cornerstone for future treatment of benign airway stenosis caused by mechanical injury.
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STING is highly expressed on macrophages and is involved in the pathogenesis of various fibrotic diseases including pulmonary fibrosis and liver fibrosis.
“Several reports have indicated that the STING is highly expressed on macrophages and is involved in the pathogenesis of various fibrotic diseases, including pulmonary fibrosis, liver fibrosis, and so on (23).”
From Matrix mechanical remodeled carrier-free nanosystem for programmable closed-loop reversal of liver fibrosis via STING alkylation (2025) · cites this paper as [23]
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Macrophage biology and immunoregulation in health and disease
Zhao, H., Chou, Y.-J., & Huang, S. C. (2026) · Cellular and Molecular Immunology · doi:10.1038/s41423-026-01486-9
- Authors
- Chen, Y., Yang, C., Miao, Y., Shi, D., Li, X., Tian, S., Zhang, Y., Xu, C., Dong, Y., Han, C., Shi, H., & Bai, C.
- Affiliations
- Chinese People's Liberation Army (CN)
- Second Military Medical University (CN)
- Corresponding author
- Han, ChaoFeng
- Shi, Hui
- Bai, Chong
- Venue
- Nature Communications
- Published
- 2025-01-03
- Volume
- 16
- Issue
- 1
- Pages
- 289-289
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC11698984
- OpenAlex
- W4406027313
- Cited by
- 51
- References
- 48
- Citations by year
- 2026: 31 · 2025: 20
- FWCI
- 18.88
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion, cc-by-nc-nd)
- Research Square (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (82270112)
- National Science Foundation of China | Young Scientists Fund (82000102)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Tracheal and airway disorders
- Health Sciences › Medicine › Pathology and Forensic Medicine › Systemic Sclerosis and Related Diseases
- Keywords
- benign airway stenosis, tracheal fibrosis, cGAS-STING pathway, macrophages, interleukin-6, STAT3, double-stranded DNA, acute and chronic inflammation, STING inhibition, macrophage depletion, epithelial damage, critically ill patients
- MeSH terms
- STING Protein, Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase, Animals, Disease Models, Animal, DNA, Epithelial Cells, Female, Fibrosis, Humans, Inflammation, Macrophages, Male, Membrane Proteins, Mice, Inbred C57BL, Nucleotidyltransferases, Trachea, Signal Transduction, Interleukin-6, Mice, Knockout, STAT3 Transcription Factor, Mice
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