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IL-24 deficiency protects mice against bleomycin-induced pulmonary fibrosis by repressing IL-4-induced M2 program in macrophages
Open accessAbstract
Idiopathic pulmonary fibrosis (IPF) is the most common type of idiopathic interstitial pneumonia and has one of the poorest prognosis. However, the molecular mechanisms underlying IPF progression remain largely unknown. In this study, we determined that IL-24, an IL-20 subfamily cytokine member, was increased both in the serum of IPF patients and the bronchoalveolar lavage fluid (BALF) of mice following bleomycin (BLM)-induced pulmonary fibrosis. As a result, IL-24 deficiency protected mice from BLM-induced lung injury and fibrosis. Specifically, loss of IL-24 significantly attenuated transforming growth factor β1 (TGF-β1) production and reduced M2 macrophage infiltration in the lung of BLM-induced mice. Mechanistically, IL-24 alone did not show a perceptible impact on the induction of M2 macrophages, but it synergized with IL-4 to promote M2 program in macrophages. IL-24 suppressed IL-4-induced expression of suppressor of cytokine signaling 1 (SOCS1) and SOCS3, through which it enhanced signal transducer and activator of transcription 6/peroxisome proliferator-activated receptor gamma (STAT6/PPARγ) signaling, thereby promoting IL-4-induced production of M2 macrophages. Collectively, our data support that IL-24 synergizes with IL-4 to promote macrophage M2 program contributing to the development of pulmonary fibrosis.
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“IPF patients are predominantly infiltrated by M2 macrophages during disease progression 12, 13.”
From Nicotinamide phosphoribosyltransferase prompts bleomycin-induced pulmonary fibrosis by driving macrophage M2 polarization in mice (2024) · cites this paper as [12]
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Metadata
- Authors
- Rao, L.-Z., Wang, Y., Zhang, L., Wu, G., Zhang, L., Wang, F.-X., Chen, L.-M., Sun, F., Jia, S., Zhang, S., Yu, Q., Wei, J.-H., Lei, H.-R., Yuan, T., Li, J., Huang, X., Cheng, B., Zhao, J., Xu, Y., Mo, B.-W., Wang, C.-Y., & Zhang, H.
- Affiliations
- Tongji Hospital (CN)
- Guilin Medical University (CN)
- Central South University (CN)
- ShanghaiTech University (CN)
- Corresponding author
- Wang, Yi
- Wang, Cong-Yi
- Zhang, Huilan
- ORCID
- Venue
- Cell Death & Differentiation
- Published
- 2020-11-03
- Volume
- 28
- Issue
- 4
- Pages
- 1270-1283
- ISSN
- 1350-9047 (ISSN-L)
- 1476-5403
- PMC
- PMC8027679
- OpenAlex
- W3095707317
- Cited by
- 153
- References
- 48
- Citations by year
- 2026: 24 · 2025: 37 · 2024: 39 · 2023: 21 · 2022: 22 · 2021: 9
- FWCI
- 7.61
- Type
- journal article
- Language
- en
- Update notices
- correction (2021-01-05)
- Open access
- bronze
- doi.org
- Locations
- Cell Death and Differentiation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81530024)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- IL-24, idiopathic pulmonary fibrosis, bleomycin-induced lung fibrosis, M2 macrophages, IL-4, SOCS1, SOCS3, TGF-β1, macrophage polarization, pulmonary fibrosis
- MeSH terms
- Interleukin-24, Animals, Bleomycin, Disease Models, Animal, Female, Humans, Interleukins, Macrophages, Male, Mice, Inbred C57BL, Pulmonary Fibrosis, Signal Transduction, Interleukin-4, Mice, Knockout, Mice, Transforming Growth Factor beta1
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