Cited by 164Interstitial Lung Diseases and Idiopathic Pulmonary FibrosisTransplantation: Methods and OutcomesCardiac Fibrosis and Remodeling

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IL-24 deficiency protects mice against bleomycin-induced pulmonary fibrosis by repressing IL-4-induced M2 program in macrophages

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Rao, Li-Zong, Wang, Yi, Zhang, Lei, Wu, Guorao, Zhang, Lu, Wang, Fa-Xi, Chen, Long-Min, Sun, Fei, Jia, Song, Zhang, Shu, Yu, Qilin, Wei, Jiang-Hong, Lei, Hui-Ren, Yuan, Ting, Li, Jinxiu, Huang, Xingxu, Cheng, Bin, Zhao, Jianping, Xu, Yongjian, Mo, Bi-Wen, Wang, Cong-Yi, Zhang, Huilan·2021·Cell Death & Differentiation

DOI 10.1038/s41418-020-00650-6PMC PMC8027679

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Abstract

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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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: Wang, Yi
Zhang, Lei
Zhang, Lu
Sun, Fei
Zhang, Shu
Yu, Qilin
Yuan, Ting
Li, Jinxiu
Huang, Xingxu
Cheng, Bin
Zhao, Jianping
Xu, Yongjian
Wang, Cong-Yi
Zhang, Huilan
Venue: Cell Death & Differentiation
Publisher: Springer Science and Business Media LLC
Published: 2020-11-03
Volume: 28
Issue: 4
Pages: 1270-1283
ISSN: 1350-9047 (ISSN-L)
1476-5403
DOI: 10.1038/s41418-020-00650-6
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
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
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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IL-24 deficiency protects mice against bleomycin-induced pulmonary fibrosis by repressing IL-4-induced M2 program in macrophages

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