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CCR2(+) 单核细胞转化修复系统可减轻缺血性脑卒中后的神经炎症。

Reparative System Arising from CCR2(+) Monocyte Conversion Attenuates Neuroinflammation Following Ischemic Stroke.

机构信息

Department of Anatomy, Yonsei University College of Medicine, Seoul, Republic of Korea.

Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea.

出版信息

Transl Stroke Res. 2021 Oct;12(5):879-893. doi: 10.1007/s12975-020-00878-x. Epub 2021 Jan 6.

DOI:10.1007/s12975-020-00878-x
PMID:33409730
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8421302/
Abstract

Monocytes recruitment from the blood to inflamed tissues following ischemic stroke is an important immune response to wound healing and tissue repair. Mouse monocytes can be endogenously divided into two distinct populations: pro-inflammatory or classical monocytes that express CCR2CX3CR1 and circulate in blood, and anti-inflammatory or non-classical monocytes that express CCR2CX3CR1 and patrol locally. In this study of transgenic mice with functional CX3CR1 or CX3CR1-CCR2, we found that CCR2CX3CR1 monocytes recruited to the injured brain were cytokine-dependently converted into CCR2CX3CR1 macrophages, especially under the influence of IL-4 and IL-13, thereby attenuating the neuroinflammation following sterile ischemic stroke. The overall data suggest that (1) the regulation of monocyte-switching is one of the ultimate reparative strategies in ischemic stroke, and (2) the adaptation of monocytes in a locally inflamed milieu is vital to alleviating the effects of ischemic stroke through innate immunity.

摘要

在缺血性中风后，单核细胞从血液招募到炎症组织中，是对伤口愈合和组织修复的重要免疫反应。小鼠单核细胞可以内部分化为两个不同的群体：表达 CCR2CX3CR1 并在血液中循环的促炎或经典单核细胞，以及表达 CCR2CX3CR1 并在局部巡逻的抗炎或非经典单核细胞。在这项针对功能性 CX3CR1 或 CX3CR1-CCR2 转基因小鼠的研究中，我们发现募集到损伤大脑的 CCR2CX3CR1 单核细胞会依赖细胞因子转化为 CCR2CX3CR1 巨噬细胞，特别是在 IL-4 和 IL-13 的影响下，从而减轻无菌性缺血性中风后的神经炎症。总的来说，这些数据表明：(1)单核细胞转换的调节是缺血性中风的最终修复策略之一；(2)在局部炎症环境中，单核细胞的适应对于通过先天免疫减轻缺血性中风的影响至关重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/84db9ba20ac1/12975_2020_878_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/33950832efed/12975_2020_878_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/8c44f9d0a770/12975_2020_878_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/9c3b684460f0/12975_2020_878_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/84db9ba20ac1/12975_2020_878_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/33950832efed/12975_2020_878_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/d56d699d8f18/12975_2020_878_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/8c44f9d0a770/12975_2020_878_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/9c3b684460f0/12975_2020_878_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/21d9/8421302/84db9ba20ac1/12975_2020_878_Fig5_HTML.jpg

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