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Updated: Jun 29, 2025

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Isolation and Culture of Primary Mouse Keratinocytes from Neonatal and Adult Mouse Skin

Published on: July 14, 2017

角质细胞中的化学素-CMKLR1轴损害了对皮肤葡萄球菌黄金菌感染的天生的宿主防御能力

Yu Chen^1,2, Yan Song³, Zhe Wang¹

¹Department of Immunology, Key Laboratory of Medical Molecular Virology (MOE/NHC), School of Basic Medical Sciences, and Shanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, 200032, China.

Cellular & molecular immunology

|March 27, 2024

概括

化学素/CMKLR1轴会损害皮肤免疫力,从而抵御黄金葡萄球菌. 阻断这个轴会增强中性粒细胞的防御能力,而过度表达则会恶化黄金色细菌的皮肤感染,特别是在肥胖患者中.

科学领域:

免疫学免疫学免疫学
皮肤病学皮肤病学
微生物学微生物学

背景情况:

金黄色葡萄球菌的皮肤感染很常见,并且可能是严重的.
皮肤中对黄金色细菌的宿主防御机制尚未完全理解.
化学素是一种皮肤蛋白质,具有免疫作用,并被S. aureus激活.

研究的目的:

为了研究化学素/CMKLR1轴在S. aureus皮肤感染中的作用.
阐明化学素影响宿主防御S. aureus的机制.
探索肥胖,化学素和黄金色杆菌敏感性之间的联系.

主要方法:

利用皮肤S. aureus感染的小鼠模型.
在缺乏或存在化学素/CMKLR1信号的情况下评估宿主防御.
研究了小鼠角质细胞中的分子机制,专注于IL-33和Akt信号传递.

主要成果:

缺乏海默林/CMKLR1轴会增强中性粒细胞介导的防御力,以抵御S. aureus.
过度表达化学素会加剧黄金色球菌的皮肤感染,模仿肥胖.
黑素/CMKLR1在角质细胞中的信号抑制S. aureus诱导的IL-33表达,损害了细菌清除.

结论:

化学素/CMKLR1轴促进S. aureus在皮肤中的免疫逃避.
这个轴通过Akt信号传递在角质细胞中抑制S. aureus诱导的IL-33产生.
化学素/CMKLR1轴的调节失调可能会增加黄金色细菌感染的易感性,特别是在肥胖个体中.

关键词:

黄金葡萄球菌黄金葡萄球菌在Chemerin-CMKLR1中使用.这里有IL-33和IL-33.角质细胞 (keratinocytes) 是一种细胞.作为一个中性粒细胞.

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