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活性氧物种调节肠道巨细胞-微生物组接口的早期发育

Zohreh Mansoori Moghadam^1,2,3, Bei Zhao^1,4,5, Candice Raynaud⁶

¹Institute for Immunodeficiency, Center for Chronic Immunodeficiency, Medical Center and Faculty of Medicine, University of Freiburg, Freiburg, Germany.

|February 3, 2025

概括

早期的肠道免疫和微生物密切相关. 尼古丁胺氨基二核酸氧化酶2 (NOX2) 的缺陷会导致自发性炎症性肠病 (IBD),当暴露于出生后复杂的微生物群时.

科学领域:

免疫学免疫学免疫学
微生物学微生物学
胃肠病学胃肠病学

背景情况:

早期发病的炎症性肠病 (IBD) 是一种严重的肠道免疫疾病.
慢性颗粒瘤性疾病 (CGD) 涉及尼古丁胺胺二核酸氧化酶2 (NOX2) 的缺陷,损害了反应性氧物种 (ROS) 的产生,并导致IBD.
在CGD中肠道免疫病理的机制尚未完全理解,部分原因是目前小鼠模型的局限性.

研究的目的:

在实验性CGD中研究肠道免疫病理学的机制.
探索NOX2缺乏,微生物群和肠道免疫发展之间的相互作用.
评估NOX2缺乏的小鼠模型对研究CGD相关IBD的有用性.

主要方法:

在化学诱导性结肠炎模型中比较p47phox和gp91phox缺乏的小鼠 (缺乏NOX2子单元).
微生物群组成的分析和交叉培养实验,以评估早期微生物群的固定.
用复杂的野生小鼠微生物群对新生儿进行殖民,以诱导NOX2缺乏小鼠的IBD和相关病理.

主要成果:

缺乏p47phox和gp91phox的小鼠对化学诱导的结肠炎表现出不同的反应,尽管基线上的巨细胞乱类似.
在NOX2缺乏的小鼠系之间,微生物群的组成有显著差异,但交叉培养并没有解决IBD表型,这表明微生物群的早期稳定.
新生儿暴露于复杂的野生小鼠微生物群诱导了自发性IBD,颗粒瘤形成和毒症在两个NOX2缺乏的线条中,部分依赖于肠道巨细胞中的NOX2.

结论:

在实验性CGD中,异常的肠组织免疫和微生物群的发展从出生就紧密交织在一起.
生命早期的环境因素,特别是微生物群的暴露,对CGD相关IBD的发展具有关键影响.
在新生儿时与复杂微生物群结合的NOX2缺乏的小鼠代表了研究CGD-IBD病变的宝贵模型.

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