Cargando…
RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway
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...
Autores principales: | , , , , , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575873/ https://www.ncbi.nlm.nih.gov/pubmed/34750369 http://dx.doi.org/10.1038/s41420-021-00708-5 |
_version_ | 1784595764559740928 |
---|---|
author | Xiang, Shu-yang Ye, Yang Yang, Qian Xu, Hao- ran Shen, Chen-xi Ma, Min-qi Jin, Shao-wu Mei, Hong-xia Zheng, Sheng-xing Smith, Fang-gao Jin, Sheng-wei Wang, Qian |
author_facet | Xiang, Shu-yang Ye, Yang Yang, Qian Xu, Hao- ran Shen, Chen-xi Ma, Min-qi Jin, Shao-wu Mei, Hong-xia Zheng, Sheng-xing Smith, Fang-gao Jin, Sheng-wei Wang, Qian |
author_sort | Xiang, Shu-yang |
collection | PubMed |
description | 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 | Online Article Text |
id | pubmed-8575873 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-85758732021-11-19 RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway Xiang, Shu-yang Ye, Yang Yang, Qian Xu, Hao- ran Shen, Chen-xi Ma, Min-qi Jin, Shao-wu Mei, Hong-xia Zheng, Sheng-xing Smith, Fang-gao Jin, Sheng-wei Wang, Qian Cell Death Discov Article 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. Nature Publishing Group UK 2021-11-08 /pmc/articles/PMC8575873/ /pubmed/34750369 http://dx.doi.org/10.1038/s41420-021-00708-5 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Xiang, Shu-yang Ye, Yang Yang, Qian Xu, Hao- ran Shen, Chen-xi Ma, Min-qi Jin, Shao-wu Mei, Hong-xia Zheng, Sheng-xing Smith, Fang-gao Jin, Sheng-wei Wang, Qian RvD1 accelerates the resolution of inflammation by promoting apoptosis of the recruited macrophages via the ALX/FasL-FasR/caspase-3 signaling pathway |
title | 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_short | 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 |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8575873/ https://www.ncbi.nlm.nih.gov/pubmed/34750369 http://dx.doi.org/10.1038/s41420-021-00708-5 |
work_keys_str_mv | AT xiangshuyang rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT yeyang rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT yangqian rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT xuhaoran rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT shenchenxi rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT maminqi rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT jinshaowu rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT meihongxia rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT zhengshengxing rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT smithfanggao rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT jinshengwei rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway AT wangqian rvd1acceleratestheresolutionofinflammationbypromotingapoptosisoftherecruitedmacrophagesviathealxfaslfasrcaspase3signalingpathway |