Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B Pathways
Macrophage-orchestrated chronic inflammation plays an important role in cardiovascular disease, including accelerating the development of calcific aortic valve disease (CAVD). M1 and M2 macrophage polarization imbalances can alter intensity of inflammatory responses. Recombinant human interleukin 37...
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| Format: | Article |
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Frontiers Media S.A.
2020-02-01
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| Series: | Frontiers in Cell and Developmental Biology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fcell.2020.00056/full |
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| author | Peitao Zhou Qianqin Li Shuwen Su Wenhui Dong Suyu Zong Qiong Ma Xi Yang Daming Zuo Shaoyi Zheng Xianzhong Meng Dingli Xu Dingli Xu Qingchun Zeng Qingchun Zeng Qingchun Zeng |
| author_facet | Peitao Zhou Qianqin Li Shuwen Su Wenhui Dong Suyu Zong Qiong Ma Xi Yang Daming Zuo Shaoyi Zheng Xianzhong Meng Dingli Xu Dingli Xu Qingchun Zeng Qingchun Zeng Qingchun Zeng |
| author_sort | Peitao Zhou |
| collection | DOAJ |
| description | Macrophage-orchestrated chronic inflammation plays an important role in cardiovascular disease, including accelerating the development of calcific aortic valve disease (CAVD). M1 and M2 macrophage polarization imbalances can alter intensity of inflammatory responses. Recombinant human interleukin 37 (IL-37) could be involved in regulating immune cell function to attenuate inflammation. This study aimed to identify IL-37 specifically modulates M1 polarization and investigate the underlying mechanism. Compared with normal valves, there are more M1 macrophages accumulation and less IL-37 expression in calcific aortic valves, which may indicate a negative relationship between IL-37 and M1 polarization. THP-1 cells could differentiate into resting macrophages with phorbol-12-myristate-13-acetate (PMA) and then polarize into M1 macrophages following treatment with lipopolysaccharide (LPS) and interferon gamma (IFN-γ). In vitro, recombinant human IL-37 attenuated the expression of inducible nitric oxide synthase (iNOS), CD11c, IL-6 and monocyte chemoattractant protein 1 (MCP-1) in M1 but augmented the expression of CD206 and IL-10 in M2. The suppression of M1 polarization was associated with the inhibition of the activation of the nuclear factor kappa B (NF-κB) and Notch1 signaling pathways. These results demonstrated that IL-37 inhibits the macrophages polarizing into M1 type via the inhibition of the Notch1 and nuclear factor kappa B pathways. In summary, IL-37 could be a potential therapeutic candidate for progressive CAVD by modulating M1 polarization and its orchestrated inflammation. |
| first_indexed | 2024-12-13T10:39:55Z |
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| issn | 2296-634X |
| language | English |
| last_indexed | 2024-12-13T10:39:55Z |
| publishDate | 2020-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cell and Developmental Biology |
| spelling | doaj.art-aca0b0883a284343b84581e62574c39d2022-12-21T23:50:35ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2020-02-01810.3389/fcell.2020.00056498458Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B PathwaysPeitao Zhou0Qianqin Li1Shuwen Su2Wenhui Dong3Suyu Zong4Qiong Ma5Xi Yang6Daming Zuo7Shaoyi Zheng8Xianzhong Meng9Dingli Xu10Dingli Xu11Qingchun Zeng12Qingchun Zeng13Qingchun Zeng14Key Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaKey Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaKey Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaKey Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaKey Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaKey Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, ChinaDepartment of Cardiovascular Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Surgery, University of Colorado Denver, Aurora, CO, United StatesKey Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaGuangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, ChinaKey Laboratory for Organ Failure Research, Department of Cardiology, Nanfang Hospital, Southern Medical University, Guangzhou, ChinaDepartment of Surgery, University of Colorado Denver, Aurora, CO, United StatesGuangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, ChinaMacrophage-orchestrated chronic inflammation plays an important role in cardiovascular disease, including accelerating the development of calcific aortic valve disease (CAVD). M1 and M2 macrophage polarization imbalances can alter intensity of inflammatory responses. Recombinant human interleukin 37 (IL-37) could be involved in regulating immune cell function to attenuate inflammation. This study aimed to identify IL-37 specifically modulates M1 polarization and investigate the underlying mechanism. Compared with normal valves, there are more M1 macrophages accumulation and less IL-37 expression in calcific aortic valves, which may indicate a negative relationship between IL-37 and M1 polarization. THP-1 cells could differentiate into resting macrophages with phorbol-12-myristate-13-acetate (PMA) and then polarize into M1 macrophages following treatment with lipopolysaccharide (LPS) and interferon gamma (IFN-γ). In vitro, recombinant human IL-37 attenuated the expression of inducible nitric oxide synthase (iNOS), CD11c, IL-6 and monocyte chemoattractant protein 1 (MCP-1) in M1 but augmented the expression of CD206 and IL-10 in M2. The suppression of M1 polarization was associated with the inhibition of the activation of the nuclear factor kappa B (NF-κB) and Notch1 signaling pathways. These results demonstrated that IL-37 inhibits the macrophages polarizing into M1 type via the inhibition of the Notch1 and nuclear factor kappa B pathways. In summary, IL-37 could be a potential therapeutic candidate for progressive CAVD by modulating M1 polarization and its orchestrated inflammation.https://www.frontiersin.org/article/10.3389/fcell.2020.00056/fullinterleukin 37macrophage polarizationNotch1NF-κBcalcific aortic valve disease |
| spellingShingle | Peitao Zhou Qianqin Li Shuwen Su Wenhui Dong Suyu Zong Qiong Ma Xi Yang Daming Zuo Shaoyi Zheng Xianzhong Meng Dingli Xu Dingli Xu Qingchun Zeng Qingchun Zeng Qingchun Zeng Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B Pathways Frontiers in Cell and Developmental Biology interleukin 37 macrophage polarization Notch1 NF-κB calcific aortic valve disease |
| title | Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B Pathways |
| title_full | Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B Pathways |
| title_fullStr | Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B Pathways |
| title_full_unstemmed | Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B Pathways |
| title_short | Interleukin 37 Suppresses M1 Macrophage Polarization Through Inhibition of the Notch1 and Nuclear Factor Kappa B Pathways |
| title_sort | interleukin 37 suppresses m1 macrophage polarization through inhibition of the notch1 and nuclear factor kappa b pathways |
| topic | interleukin 37 macrophage polarization Notch1 NF-κB calcific aortic valve disease |
| url | https://www.frontiersin.org/article/10.3389/fcell.2020.00056/full |
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