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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Autores principales: 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
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Publicado: Nature Publishing Group 2021
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spelling 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)
institution DOAJ
collection DOAJ
language EN
topic Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Cytology
QH573-671
spellingShingle 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
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