在高海拔地区缺氧时,肠道菌群调节的新机制
Fang Yan1,2, Wen-Qiang Yuan1,2, Shi-Min Wu1,3
1Department of Gastroenterology, National Institution of Drug Clinical Trial, Guizhou Provincial People's Hospital, No.83, East Zhongshan Road, Guiyang, Guizhou, China.
Heliyon
|November 5, 2024
概括
菲尔米库特细菌通过抑制HIF-1α/糖解路径,重编程巨细胞两极分化来减轻高海拔低氧损伤. 这种作用减轻了肠粘膜屏障损伤,改善了缺氧症状.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 生理学 生理学 生理学
背景情况:
- 高海拔低氧诱导肠道粘膜屏障损伤.
- 巨细胞 (Mψ) 两极分化和糖溶性重编程与这种损伤有关.
- 研究了Firmicutes在调节这些过程中的作用.
研究的目的:
- 为了阐明Firmicutes介导的Mψ极化和在高海拔低氧下代谢重编程的分子机制.
- 为了确定关键的信号通路和代谢物参与肠粘膜屏障损伤.
- 为了验证Firmicutes在减轻缺氧引起的损伤方面的治疗潜力.
主要方法:
- 建立了一个高海拔低氧小鼠模型.
- 利用了单细胞转录组学,蛋白组学和代谢组学.
- 通过RAW264.7 Mψ进行了体外测试,并通过Firmicutes移植进行了体内验证.
- 采用了组织学分析,FITC-dextran测定和分子技术 (流细胞计,免疫光学,ELISA,西斑,RT-qPCR).
主要成果:
- 单细胞转录组学发现Mψ两极化在缺氧诱导的屏障损伤中至关重要.
- 在这个过程中,HIF-1α和糖溶性通路被确定为关键.
- 菲尔米库特的代谢物黄油酸抑制了HIF-1α/糖解路径,抑制了M1 Mψ两极化,并激活了M2 Mψ两极化.
- 在体内实验证实Firmicutes在缺氧小鼠中减轻了肠道屏障损伤.
结论:
- 菲尔米库特抑制HIF-1α/糖解路径以调节Mψ极化.
- 这种调制可缓解高海拔低氧时肠粘膜屏障损伤.
- 坚固的树木代表了与高海拔相关的疾病的潜在治疗策略.
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