Bsep/Abcb11淘汰赛通过减少寄生虫生育能力来改善Schistosoma mansoni肝脏病理
Tomáš Macháček1,2, Claudia D Fuchs3, Franziska Winkelmann1
1Division of Tropical Medicine and Infectious Diseases, Center of Internal Medicine II, Rostock University Medical Center, Rostock, Germany.
概括
在 Schistosoma mansoni 感染后,缺乏胆汁载体 Bsep 的小鼠表现出肝炎和纤维化减少. 这表明胆酸的变化可能会防止寄生虫诱导的肝损伤.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 寄生虫学的寄生虫学
- 免疫学 免疫学 免疫学
背景情况:
- 在全球范围内,schistosoma mansoni感染是肝纤维化和门性高血压的主要原因.
- 众所周知,多氧化胆汁酸 (BAs) 有助于防止胆固醇性肝损伤.
- 这项研究调查BA是否可以减轻S. mansoni诱导的肝炎和纤维化.
研究的目的:
- 为了评估改变胆酸组成对schistosoma mansoni感染的保护作用.
- 评估Bsep缺乏对小鼠肝脏病理和寄生虫负载的影响.
主要方法:
- 成年野生型 (WT) 和ABCB11/Bsep-/-小鼠感染了S. mansoni.
- 肝脏组织学,血清生物化学,基因表达和细胞分析在感染后8周进行.
主要成果:
- 与WT小鼠相比,Bsep-/-小鼠表现出明显减少的肝炎和较少纤维化趋势.
- 尽管肝酶升高,但Bsep-/-小鼠的炎症细胞 (M2巨细胞,Mac-2+) 减少,抗炎细胞因子 (IL-4,IL-13) 增加.
- 受感染的Bsep-/-小鼠的肝卵负荷和寄生虫生育能力较低,可能是由于血清BAA升高和血液pH降低.
结论:
- 失去Bsep功能会改变胆酸成分和血液pH值,降低寄生虫的生育能力.
- 这些变化减轻了S. mansoni诱导的肝炎和纤维化的发展.
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