在转化性结肠炎小鼠模型中,受损的Abcb1a功能和红肉诱导炎症并改变微生物群组成
Allan Stensballe1,2, Tue Bjerg Bennike1, Gitte Ravn-Haren3
1Department of Health Science and Technology, Aalborg University, Aalborg, Denmark.
Frontiers in medicine
|August 17, 2023
概括
药物载体缺乏会改变肠道微生物群,增加与炎症性肠病 (IBD) 相关的细菌,并在小鼠模型中引起肠道炎症. 这凸显了排泄在IBD病变发生过程中的作用.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 微生物组研究 微生物组研究
背景情况:
- 炎症性肠病 (IBD) 影响全球数百万人,与饮食,遗传和免疫系统相互作用相关的发病率不断增加.
- 像p-glycoprotein (Abcb1) 一样,ATP结合盒 (ABC) 载体与肠道炎症有关,并且可能与环境因素相互作用.
- 了解宿主基因,饮食和微生物群之间的相互作用对于IBD发展至关重要.
研究的目的:
- 研究饮食蛋白质来源对大肠炎遗传小鼠模型的影响.
- 检查Abcb1a缺乏和红肉补充饮食如何影响宿主微生物群相互作用和肠道炎症.
主要方法:
- 使用的ABCb1a缺乏性大肠炎小鼠被食素或红肉补充饮食.
- 对胃肠组织和尿液进行了定量蛋白质组分析.
- 使用16S rRNA基因测序评估便微生物组合,并通过组织学和免疫分析验证炎症.
主要成果:
- 缺乏abcb1a和饮食显著改变了肠道微生物组的组成.
- 蛋白质组分析揭示了与Abcb1a缺陷相关的阴茎和尿液蛋白质之间的关联.
- 中性粒细胞外细胞陷 (NET) 成分升高,表明系统性免疫激活和中性粒细胞脱粒化.
结论:
- 药物载体缺乏严重影响肠道微生物群,增加IBD相关的细菌菌株.
- 这种小鼠模型的见解,特别是关于NETs的见解,可能为人类IBD提供翻译生物标志物.
- 这项研究增强了对IBD病原学的理解,强调了排泄输送物在宿主-微生物群-免疫系统相互作用中的作用.
关键词:
Abcb1 Abcb1 是一个字母.网络 网络 网络 网络结肠 粘膜 结肠 粘膜饮食 饮食 饮食 饮食我们的微生物群.中性粒细胞的脱粒化.这是一种p-glycoprotein蛋白.蛋白质组学 蛋白质组学更多相关视频
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