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马雷斯汀 1-LGR6 轴可降低呼吸道合胞病毒诱导的肺部炎症。

The Maresin 1-LGR6 axis decreases respiratory syncytial virus-induced lung inflammation.

机构信息

Pulmonary and Critical Care Medicine Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.

Neonatology Division, Mass General Hospital for Children, Boston, MA 02114.

出版信息

Proc Natl Acad Sci U S A. 2023 Jan 10;120(2):e2206480120. doi: 10.1073/pnas.2206480120. Epub 2023 Jan 3.

DOI:10.1073/pnas.2206480120
PMID:36595677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9926266/
Abstract

The resolution of infection is an active process with specific molecular and cellular mechanisms that temper inflammation and enhance pathogen clearance. Here, the specialized pro-resolving mediator (SPM) Maresin 1 (MaR1) inhibited respiratory syncytial virus (RSV)-induced inflammation. inlerleukin-13 production from type 2 innate lymphoid cells (ILC) and CD4 T helper type 2 cells was decreased by exogenous MaR1. In addition, MaR1 increased amphiregulin production and decreased RSV viral transcripts to promote resolution. MaR1 also promoted interferon-β production in mouse lung tissues and also in pediatric lung slices. MaR1 significantly inhibited the RSV-triggered aberrant inflammatory phenotype in FoxP3-expressing Tregs. The receptor for MaR1, leucine-rich repeat-containing G protein-coupled receptor 6 (LGR6), was constitutively expressed on Tregs. Following RSV infection, mice lacking Lgr6 had exacerbated type 2 immune responses with an increased viral burden and blunted responses to MaR1. Together, these findings have uncovered a multi-pronged protective signaling axis for MaR1-Lgr6, improving Tregs's suppressive function and upregulating host antiviral genes resulting in decreased viral burden and pathogen-mediated inflammation, ultimately promoting restoration of airway mucosal homeostasis.

摘要

感染的解决是一个积极的过程，具有特定的分子和细胞机制，可以调节炎症并增强病原体清除。在这里，特异性促解决介质（SPM）maresin 1（MaR1）抑制呼吸道合胞病毒（RSV）诱导的炎症。外源性 MaR1 可减少 2 型先天淋巴样细胞（ILC）和 CD4 T 辅助 2 型细胞产生白细胞介素 13（IL-13）。此外，MaR1 增加 Amphiregulin 的产生并减少 RSV 病毒转录物以促进解决。MaR1 还可促进鼠肺组织和儿科肺切片中的干扰素-β产生。MaR1 还显著抑制了 FoxP3 表达的 Treg 中 RSV 触发的异常炎症表型。MaR1 的受体富含亮氨酸重复的 G 蛋白偶联受体 6（LGR6）在 Treg 上持续表达。在 RSV 感染后，缺乏 Lgr6 的小鼠表现出 2 型免疫反应加剧，病毒载量增加，对 MaR1 的反应减弱。总之，这些发现揭示了 MaR1-Lgr6 的多方面保护信号轴，改善了 Treg 的抑制功能，并上调了宿主抗病毒基因，从而降低了病毒载量和病原体介导的炎症，最终促进气道黏膜稳态的恢复。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/cca22948629f/pnas.2206480120fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/720cd79303c3/pnas.2206480120fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/fd91f1ab0a4e/pnas.2206480120fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/dc351d7a3124/pnas.2206480120fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/18de474c88d7/pnas.2206480120fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/6df062f6a83a/pnas.2206480120fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/cca22948629f/pnas.2206480120fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/720cd79303c3/pnas.2206480120fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/fd91f1ab0a4e/pnas.2206480120fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/dc351d7a3124/pnas.2206480120fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/18de474c88d7/pnas.2206480120fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/6df062f6a83a/pnas.2206480120fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d0c5/9926266/cca22948629f/pnas.2206480120fig06.jpg

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