RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway
Abstract The uncontrolled inflammatory response caused by a disorder in inflammation resolution is one of the reasons for acute respiratory distress syndrome (ARDS). The macrophage pool markedly expands when inflammatory monocytes, known as recruited macrophages, migrate from the circulation to the...
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Nature Publishing Group
2021
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oai:doaj.org-article:639cb9e1364a4757bb0a5a282446cc522021-11-14T12:12:30ZRvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway10.1038/s41420-021-00708-52058-7716https://doaj.org/article/639cb9e1364a4757bb0a5a282446cc522021-11-01T00:00:00Zhttps://doi.org/10.1038/s41420-021-00708-5https://doaj.org/toc/2058-7716Abstract The uncontrolled inflammatory response caused by a disorder in inflammation resolution is one of the reasons for acute respiratory distress syndrome (ARDS). The macrophage pool markedly expands when inflammatory monocytes, known as recruited macrophages, migrate from the circulation to the lung. The persistent presence of recruited macrophages leads to chronic inflammation in the resolution phase of inflammation. On the contrary, elimination of the recruited macrophages at the injury site leads to the rapid resolution of inflammation. Resolvin D1 (RvD1) is an endogenous lipid mediator derived from docosahexaenoic acid. Mice were administered RvD1 via the tail vein 3 and 4 days after stimulation with lipopolysaccharide. RvD1 reduced the levels of the inflammatory factors in the lung tissue, promoted the anti-inflammatory M2 phenotype, and enhanced the phagocytic function of recruited macrophages to alleviate acute lung injury. We also found that the number of macrophages was decreased in BAL fluid after treatment with RvD1. RvD1 increased the apoptosis of recruited macrophages partly via the FasL-FasR/caspase-3 signaling pathway, and this effect could be blocked by Boc-2, an ALX/PRP2 inhibitor. Taken together, our findings reinforce the concept of therapeutic targeting leading to the apoptosis of recruited macrophages. Thus, RvD1 may provide a new therapy for the resolution of ARDS.Shu-yang XiangYang YeQian YangHao- ran XuChen-xi ShenMin-qi MaShao-wu JinHong-xia MeiSheng-xing ZhengFang-gao SmithSheng-wei JinQian WangNature Publishing GrouparticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282CytologyQH573-671ENCell Death Discovery, Vol 7, Iss 1, Pp 1-10 (2021) |
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Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Cytology QH573-671 |
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Neoplasms. Tumors. Oncology. Including cancer and carcinogens RC254-282 Cytology QH573-671 Shu-yang Xiang Yang Ye Qian Yang Hao- ran Xu Chen-xi Shen Min-qi Ma Shao-wu Jin Hong-xia Mei Sheng-xing Zheng Fang-gao Smith Sheng-wei Jin Qian Wang RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway |
description |
Abstract The uncontrolled inflammatory response caused by a disorder in inflammation resolution is one of the reasons for acute respiratory distress syndrome (ARDS). The macrophage pool markedly expands when inflammatory monocytes, known as recruited macrophages, migrate from the circulation to the lung. The persistent presence of recruited macrophages leads to chronic inflammation in the resolution phase of inflammation. On the contrary, elimination of the recruited macrophages at the injury site leads to the rapid resolution of inflammation. Resolvin D1 (RvD1) is an endogenous lipid mediator derived from docosahexaenoic acid. Mice were administered RvD1 via the tail vein 3 and 4 days after stimulation with lipopolysaccharide. RvD1 reduced the levels of the inflammatory factors in the lung tissue, promoted the anti-inflammatory M2 phenotype, and enhanced the phagocytic function of recruited macrophages to alleviate acute lung injury. We also found that the number of macrophages was decreased in BAL fluid after treatment with RvD1. RvD1 increased the apoptosis of recruited macrophages partly via the FasL-FasR/caspase-3 signaling pathway, and this effect could be blocked by Boc-2, an ALX/PRP2 inhibitor. Taken together, our findings reinforce the concept of therapeutic targeting leading to the apoptosis of recruited macrophages. Thus, RvD1 may provide a new therapy for the resolution of ARDS. |
format |
article |
author |
Shu-yang Xiang Yang Ye Qian Yang Hao- ran Xu Chen-xi Shen Min-qi Ma Shao-wu Jin Hong-xia Mei Sheng-xing Zheng Fang-gao Smith Sheng-wei Jin Qian Wang |
author_facet |
Shu-yang Xiang Yang Ye Qian Yang Hao- ran Xu Chen-xi Shen Min-qi Ma Shao-wu Jin Hong-xia Mei Sheng-xing Zheng Fang-gao Smith Sheng-wei Jin Qian Wang |
author_sort |
Shu-yang Xiang |
title |
RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway |
title_short |
RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway |
title_full |
RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway |
title_fullStr |
RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway |
title_full_unstemmed |
RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway |
title_sort |
rvd1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the alx/fasl-fasr/caspase-3 signaling pathway |
publisher |
Nature Publishing Group |
publishDate |
2021 |
url |
https://doaj.org/article/639cb9e1364a4757bb0a5a282446cc52 |
work_keys_str_mv |
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