肠道微生物分泌物可能触发单核细胞迁移,并在炎症性肠病和糖尿病视网膜病变之间提供并发症机制
Bingyu Xu1, Shuduan Wu2,3, Junfei Huang1
1The Second Clinical School, Southern Medical University, Guangzhou, Guangdong, China.
Mediators of inflammation
|December 3, 2025
概括
肠道微生物及其炎症分泌物,如胆酸,有助于炎症性肠病 (IBD) 和糖尿病视网膜病变 (DR) 的并发症. 这项研究揭示了肠道失调如何加剧视网膜炎症和DR进展.
科学领域:
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
- 眼科医生 眼科 眼科
背景情况:
- 肠道微生物群通过分泌的化学物质,如胆酸 (BAs) 和L-kynurenine,影响炎症.
- 研究肠道微生物及其分泌物在炎症性肠病 (IBD) 和糖尿病视网膜病变 (DR) 并发症中的作用至关重要.
研究的目的:
- 分析IBD和糖尿病患者的特定肠道微生物.
- 为了确定这些微生物分泌的促炎化学物质.
- 阐明肠道微生物及其分泌物在IBD-DR并发症机制中的功能性作用.
主要方法:
- 在IBD和DM患者中分析肠道微生物群和分泌的化学物质.
- 对外围血液单核细胞 (PBMC) 的基因表达分析 (DEG,WGCNA).
- 单细胞分析以了解并发症的细胞学机制.
主要成果:
- 异常肠道微生物 (例如,BA,L-Kynurenine) 的分泌物刺激异常免疫反应.
- 来自失生性肠道微生物群 (Veillonella,Clostridium) 的促炎物质激活PBMCs,破坏血管屏障,并恶化DR.
- 促进PBMC迁移的基因 (RSU1,FN1,CD9) 被激活,显示出一种遗传性并发症机制.
- IBD促进效应记忆T (Tem) 细胞的增殖和激活,在DR中也升高,为并发症提供细胞基础.
结论:
- IBD患者的异常肠道细菌分泌有助于炎症的物质,激活单核细胞,特别是Tem细胞.
- 激活的单核细胞迁移到视网膜,加剧了DR.
- 了解这种肠-视网膜轴为DR治疗提供了潜在的治疗策略.
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