慢性高血糖症损害了巨细胞的抗微生物功能,以应对Mycobacterium结核病感染
Gaurav Kumar Chaubey1, Radheshyam Modanwal1, Rahul Dilawari1
1Institute of Microbial Technology, CSIR, Sector 39A, Chandigarh, 160036, India.
Immunologic research
|February 12, 2024
概括
高血糖会损害巨细胞对结核病 (TB) 的免疫防御. 糖尿病巨体显示反应性氧物种 (ROS) 和促炎性细胞因子的产生减少,增加对Mycobacterium结核病 (Mtb) 感染的易感性.
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:
- 糖尿病 (DM) 是结核病 (TB) 的重要危险因素,但其机制尚未完全理解.
- 巨细胞对于天生的免疫力至关重要,产生ROS,RNS和细胞因子来对抗病原体.
- 过高血糖对巨细胞对Mycobacterium tuberculosis (Mtb) 防御功能的影响需要进一步研究.
研究的目的:
- 研究高血糖症对巨细胞产生宿主防御分子的影响.
- 探索糖尿病患者中Mtb易感性增加的潜在机制.
主要方法:
- 从糖尿病小鼠和高血糖THP-1衍生的巨细胞中利用了腹巨细胞.
- 刺激的巨细胞与Mycobacterium结核病 (Mtb) 感染和脂多糖 (LPS).
- 测量了ROS,RNS,促炎性 (IL-1β,IL-6) 和抗炎性 (IL-10) 细胞因子的产生.
- 评估了巨细胞激活和分化标志物 (TLR-4,CD11b,CD11c).
主要成果:
- 高血糖症显著降低了ROS,RNS和促炎细胞因子的产生,以应对Mtb和LPS.
- 在高血糖性巨细胞中观察到抗炎性细胞因子生产的增加.
- 糖尿病巨细胞表现出激活 (TLR-4) 和分化标记物的表面表达减少 (CD11b,CD11c).
结论:
- 过高血糖会损害巨细胞的先天免疫反应,损害它们对抗Mtb感染的能力.
- 降低关键防御分子的产生和激活标记物的表达减少有助于糖尿病患者对结核病的易感性增加.
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