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微生物肠道失生症通过塑造ILC2-B1细胞天生的IgE轴来驱动长期的过敏敏感性

Ahmed Kabil¹, Natalia Nayyar¹, Julyanne Brassard¹

¹School of Biomedical Engineering, University of British Columbia, Vancouver, British Columbia, Canada.

The Journal of allergy and clinical immunology

|August 12, 2024

概括

在生命早期肠道细菌的枯竭增加了2型过敏性肺病的易感性. 短链脂肪酸 (SCFA) 调节这种免疫轴,SCFA 补充剂可以逆转这些影响.

科学领域:

免疫学免疫学免疫学
微生物组研究微生物组研究
过敏和喘过敏和喘

背景情况:

肠道共生细菌显著影响系统免疫力,影响疾病的易感性和严重性.
早期生命中短链脂肪酸 (SCFA) 发酵细菌的丧失与肺部等外围组织的2型免疫反应加剧有关.

研究的目的:

阐明微生物组依赖的细胞和分子机制,是导致2型过敏性肺部疾病的增加易感性的基础.
研究SCFA在调节与过敏性肺炎相关的免疫反应中的作用.

主要方法:

在小鼠中使用低剂量的万科米辛来选择性地消耗SCFA发酵细菌.
评估先天性和适应性免疫细胞群和激活状态,有或没有SCFA补充剂.
采用ILC2缺乏和STAT6缺乏的小鼠模型来定义关键的细胞和细胞因子通路.

主要成果:

范科米辛诱导的失生症导致肺部第2组先天性淋巴细胞 (ILC2s) 增加了两倍,这些细胞为IL-2, -5,和 -13生产提供了原料.
肺部ILC2s在吸入IL-33时表现出前所未有的IL-4产生能力.
扩大的ILC2s促进了B1细胞扩张和依赖IL-4的IgE产生,加剧了过敏性炎症;饮食中的SCFA (丁酸盐) 逆转了这些影响.

结论:

短链脂肪酸 (SCFA) 是ILC2-B1细胞-IgE免疫轴的关键调节剂.
早期抗生素诱导的SCFA发酵细菌的枯竭原始化和放大了这一轴,导致终身易受2型过敏性肺病的影响.

关键词:

B1 细胞 B1 细胞在 ILC2 中.短链脂肪酸短链脂肪酸过敏性肺炎过敏性肺炎我们的肠道微生物组.天生的天然IgE.

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