在结核病与糖尿病接触时,人脉膜巨功能受损
Léanie Kleynhans1,2,3, Carine Kunsevi-Kilola1, Happy Tshivhula1
1DSI-NRF Centre of Excellence for Biomedical Tuberculosis Research, SA MRC Centre for TB Research, Division of Molecular Biology and Human Genetics, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Stellenbosch University, Cape Town, South Africa.
Research square
|December 9, 2024
概括
2型糖尿病 (T2D) 由于肺免疫细胞功能障碍,使结核病 (TB) 风险恶化. T2D 损害了膜巨对 Mycobacterium 结核病的反应,增加了细菌生长和结核病的严重程度.
科学领域:
- 免疫学 免疫学 免疫学
- 传染性疾病 传染性疾病
- 代谢障碍 代谢障碍 代谢障碍
背景情况:
- 2型糖尿病 (T2D) 是已知的结核病 (TB) 的风险因素.
- 关联T2D与增加结核病易感性的特定免疫机制尚未完全理解.
- 肺部免疫细胞,特别是巨细胞,在防治结核病方面发挥着至关重要的作用.
研究的目的:
- 研究T2D和结核病暴露的个体中肺免疫细胞功能障碍的作用.
- 为了比较T2D和非T2D个体在Mycobacterium结核病 (M.tb) 感染时的膜巨细胞 (HAMs) 和单细胞衍生巨细胞 (MDMs) 的功能.
主要方法:
- 从有或没有T2D的结核病暴露个体中分离出配对的HAM和MDM.
- 巨被M.tb感染,并评估了细菌生长,细胞因子生产 (TNF,IL-1RA,CSF2) 和细胞表面标记物表达 (CD32,M1-like).
- 分析了支气管膜洗液中中性粒细胞的数量.
- 研究了HAMs中的基因表达和DNA甲基化模式.
主要成果:
- 与对照组相比,T2D-HAMs表现出增加的M.tb增长和更高的TNF产生.
- 在T2D患者的支气管支气管洗中观察到较少的中性粒细胞,与M.tb生长相反相关.
- T2D-HAMs和MDMs显示CD32表达减少,而T2D患者的M1型MDMs较少.
- 在T2D-HAMs中,M.tb诱导的基因表达被延迟,对基因的上调调节负面调节中性粒细胞迁移.
- T2D-HAM DNA显示过甲基化,而与TNF信号相关的基因被低甲基化.
结论:
- 肺巨中的T2D相关的免疫功能障碍有助于增加结核病的易感性和严重性.
- 变化的巨细胞功能,减少中性粒细胞的存在,以及T2D中的表观遗传变化可能解释了结核病风险的增加.
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