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皮肤菌群依赖的巨噬细胞亚群可预防皮肤细菌感染。

A Microbiota-Dependent Subset of Skin Macrophages Protects Against Cutaneous Bacterial Infection.

机构信息

Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea.

Department of Dermatology, Ajou University School of Medicine, Suwon, South Korea.

出版信息

Front Immunol. 2022 Jun 9;13:799598. doi: 10.3389/fimmu.2022.799598. eCollection 2022.

DOI:10.3389/fimmu.2022.799598
PMID:35757750
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9218056/
Abstract

Microbiota is essential to the development and functional maturation of the immune system. The effects of the gut microbiota on myeloid cells remote from the gut, especially the skin remain unclear. Transcriptomic analysis revealed that type I interferon (IFN) signaling was down-regulated in the skin of germ-free mice compared to that in specific pathogen-free mice. The decrease in type I IFN signaling was closely related to the presence of microbiota and macrophage-specific marker CD169. The absence of CD169 macrophages resulted in increased bacterial burden and impaired immune responses against Staphylococcus aureus skin infection. CD169 macrophages mediated the recruitment of γδ T cells as well as the activation of γδ T cells via interleukin (IL)-23. Our findings demonstrate the role of the microbiota in establishment of a specific myeloid cell subset expressing CD169 in the skin and provide evidence of a specific mechanism by which this subset protects against bacterial skin infection.

摘要

微生物组对于免疫系统的发育和功能成熟至关重要。肠道微生物组对肠道以外的髓系细胞（尤其是皮肤）的影响尚不清楚。转录组分析显示，与无特定病原体小鼠相比，无菌小鼠皮肤中的 I 型干扰素（IFN）信号下调。I 型 IFN 信号的降低与微生物组和巨噬细胞特异性标志物 CD169 的存在密切相关。缺乏 CD169 巨噬细胞会导致细菌负荷增加，并损害对金黄色葡萄球菌皮肤感染的免疫反应。CD169 巨噬细胞通过白细胞介素（IL）-23 介导 γδ T 细胞的募集和激活。我们的研究结果表明，微生物组在皮肤中建立表达 CD169 的特定髓系细胞亚群中的作用，并提供了该亚群抵御细菌皮肤感染的特定机制的证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/4e12dee15b1d/fimmu-13-799598-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/6a679dd27af6/fimmu-13-799598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/484347d42798/fimmu-13-799598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/6e4882a84eaa/fimmu-13-799598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/814aa9cce7ab/fimmu-13-799598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/8a8ca919b3eb/fimmu-13-799598-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/4e12dee15b1d/fimmu-13-799598-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/6a679dd27af6/fimmu-13-799598-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/484347d42798/fimmu-13-799598-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/6e4882a84eaa/fimmu-13-799598-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/814aa9cce7ab/fimmu-13-799598-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/8a8ca919b3eb/fimmu-13-799598-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7e9d/9218056/4e12dee15b1d/fimmu-13-799598-g006.jpg

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