胰岛素通过肠道微生物群调节和MyD88/IL-18信号传递来加剧结肠炎
Xu Zhao1, Yadong Wang1, Yanling Wang1
1Center for Inflammation, Immunity and Infection, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA, USA.
在结肠炎模型中,胰岛素纤维通过改变肠道微生物群,增加促炎信号和影响后代来恶化肠道炎症. 这凸显了对肠道健康的饮食干预中需要仔细选择纤维的必要性.
科学领域:
- 胃肠病学 胃肠病学
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 食纤维显著影响肠道微生物群的组成和宿主健康.
- 不同的纤维类型,如胰岛素,对炎症状况的具体影响仍然不完全理解.
研究的目的:
- 为了研究胰岛素补充剂对肠道炎症的影响,硫酸 (DSS) 诱导的大肠炎的小鼠模型.
- 阐明胰岛素对肠道微生物群和炎症影响的机制.
主要方法:
- 使用DSS诱导的大肠炎小鼠模型.
- 管理的胰岛素补充剂.
- 评估肠道微生物群的组成,细菌负载和多样性.
- 分析了炎症标志物和免疫细胞参与 (GR-1+细胞).
- 使用转基因小鼠 (NLRC4/TLR5-,MyD88-,IL-18淘汰) 来识别关键的信号通路.
主要成果:
- 胰岛素以肠道微生物群依赖的方式加剧了DSS诱导的大肠炎.
- 胰岛素增加了细菌负载,扩大了亲结肠炎病原体,增加了鞭毛素水平,并减少了微生物多样性.
- 大肠炎的恶化是由GR-1+细胞炎症,通过MyD88传递鞭毛蛋白信号以及IL-18炎症酶激活的介导.
- 哺乳期间母亲的胰岛素消费增加了后代对结肠炎的敏感性.
结论:
- 胰岛素摄入会通过微生物群调节和MyD88/IL-18信号通路加剧DSS诱导的大肠炎.
- 这些对肠道健康的有害影响可以传给后代.
- 饮食干预应考虑纤维类型及其对肠道微生物群多样性的影响,以获得最佳的肠道健康.
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