在结核病接触者与糖尿病患者之间,人类大膜巨细胞功能受损
Léanie Kleynhans1, Carine Kunsevi-Kilola2, Happy Tshivhula2
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; Mater Research Institute - The University of Queensland, Translational Research Institute, Brisbane, QLD, Australia; Australian Infectious Diseases Research Centre, The University of Queensland, Brisbane, QLD, Australia.
2型糖尿病 (T2D) 损害了对Mycobacterium tuberculosis (Mtb) 的早期人膜巨细胞 (HAM) 反应,增加了Mtb的生长. 这种糖尿病HAM表型涉及延迟基因表达,表观遗传变化和减少中性粒细胞的招募,解释了T2D患者的结核病风险增加.
科学领域:
- 免疫学 免疫学 免疫学
- 传染性疾病 传染性疾病
- 内分泌学 在内分泌学.
背景情况:
- 结核病 (TB) 不成比例地影响2型糖尿病 (T2D) 患者,导致严重疾病和不良结果.
- 与T2D相关的结核病敏感性增加背后的机制尚不清楚.
研究的目的:
- 调查T2D在早期的Mycobacterium结核病 (Mtb) 感染期间对人类大膜巨细胞 (HAM) 功能的影响.
- 阐明导致T2D患者结核病风险增加的细胞和分子机制.
主要方法:
- 支气管洗液 (BAL) 和配对的人类支气管巨细胞 (HAMs) 和单细胞衍生巨细胞 (MDMs) 从有和没有T2D的结核病接触者中收集.
- 细胞在体外MTB感染后进行了转录组,表观遗传和功能测试.
主要成果:
- T2D-HAMs表现出增加的Mtb生长和增加的TNF产生.
- 来自T2D患者的BAL液显示中性粒细胞数量减少,与Mtb增长相反相关.
- T2D巨体显示了改变的CD32表达,较少的M1-样巨体,延迟的Mtb诱导的基因表达和表观遗传修饰.
结论:
- T2D显著改变了对Mtb的早期HAM反应,其特征是基因转录延迟,细胞因子的表观遗传失调和中性粒细胞招募受损.
- 这些T2D诱导的巨细胞变化集体增强了Mtb的生长,提供了对T2D患者结核病易感性增加的机制性见解.
相关概念视频
Pulmonary Tuberculosis I
Causative Organism
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Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
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Latent tuberculosis infection occurs when TB bacteria are present in a person's body, but are not causing illness or symptoms. It is not contagious, and preventive treatment is crucial to avoid the...
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The first classification is based on the development of the disease, and it includes the following categories:
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
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