基基基因 IL-4 和 IL-13 保护肠道屏障的完整性,并在疟疾期间控制细菌转移
Nora Céspedes1, Abigail M Fellows1, Erinn L Donnelly2
1Department of Entomology, Plant Pathology and Nematology, University of Idaho, Moscow, ID.
ImmunoHorizons
|May 23, 2024
概括
基基基基因的IL-4和IL-13对于在疟疾感染期间保持肠道屏障完整性至关重要. 这些细胞因子阻止杆细胞激活和细菌转移,但不会影响寄生虫的传播.
科学领域:
- 免疫学 免疫学 免疫学
- 寄生虫学的寄生虫学
- 胃肠病学 胃肠病学
背景情况:
- 基细胞是疟疾表型的关键调节者,包括肠道炎症和寄生虫传播.
- 激活的基因细胞是白内素-4 (IL-4) 和白内素-13 (IL-13) 的主要来源,它们是关键的调节性细胞因子.
研究的目的:
- 研究基基基基基因 IL-4 和 IL-13 在调节疟疾相关表型中的作用.
- 确定这些细胞因子对肠道屏障完整性和寄生虫传播的贡献.
主要方法:
- 通过使用mcpt8-Cre和Il4/Il13fl/fl交叉,产生基细胞缺乏IL-4和IL-13 (基 IL-4/IL-13 (-)) 的小鼠.
- 这些小鼠和对照 littermates (基于IL-4/IL-13 (+)) 感染了Plasmodium yoelii yoelii 17XNL.
- 评估肠道巨细胞症,透性,细菌转移 (16S水平) 和寄生虫传播.
主要成果:
- 基细胞中IL-4/IL-13的有条件删除导致了以利亚性巨细胞症,巨细胞激活和肠道透性增加.
- 在巴索IL-4/IL-13 (-) 鼠群中观察到血液中的细菌16S水平增加,表明细菌转位的控制受损.
- 基基基因的IL-4和IL-13并没有影响中性粒细胞的激活,寄生虫病或向Anopheles stephensi.传染.
结论:
- 基基基基因的IL-4和IL-13对于在Plasmodium yoelii感染期间保护肠道屏障完整性至关重要.
- 这些细胞因子调节巨细胞的激活,并防止感染引起的肠损伤和细菌血症.
- 这些发现表明基因细胞IL-4/IL-13在调节氨基细胞,巨细胞和Th17介导的炎症中的作用.
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