细菌的细胞外囊泡 Bacteroides fragilis 通过促进Sema7a表达调节了巨细胞的两极分化
Cong Chen1, Yu-Qi He1, Yan Gao2
1The First Affiliated Hospital, Department of Laboratory Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Microbial pathogenesis
|January 1, 2024
概括
肠道 Bacteroides fragilis 细胞外囊泡 (EV) 驱动巨细胞极化,这是2型糖尿病的关键因素. 这项研究确定了调节这一过程的Sting-Sgpl1-Sema7a通路,提供了新的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 代谢疾病 代谢疾病
背景情况:
- 巨分化和肠道Bacteroides fragilis (BF) 与2型糖尿病 (T2D) 和血管并发症有关.
- 在巨细胞两极分化中BF的具体作用尚不清楚.
研究的目的:
- 研究BF细胞外囊泡 (EV) 影响巨细胞极化的机制.
- 识别BF-EV介导的巨分化调节中的关键分子参与者.
主要方法:
- 大细胞对BF-EV的吸收得到证实.
- 分析了巨细胞两极分化 (M1/M2) 和基因表达 (Sting,Sema7a,Sgpl1).
- 使用生物信息学分析和药理抑制 (C-176).
主要成果:
- BF-EV促进巨细胞M1/M2两极分化,并增加刺痛的表达.
- BF-EV诱导Sema7a表达,而Sema7a表达被C-176抑制,从而防止极化.
- BF-EV上调Sgpl1,它与Sting和Sema7a相互作用,调解了BF-EV的影响.
结论:
- BF-EV通过Sting-Sgpl1-Sema7a信号轴调节巨细胞的两极分化.
- 在T2D发育的背景下,这种途径对BF诱导的巨细胞极化至关重要.
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