单碳酸盐载体4通过NF-κB p65介导的介素-10生产促进了Mycobacterium tuberculosis的生存
Yingqi Huang1,2, Rong Li1,2, Shuo Chen1,2
1Institute of Molecular Immunology, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou 510515, China.
iScience
|August 7, 2024
概括
单碳酸盐载体4 (Mct4) 通过促进乳酸出口来提高结核病的存活率,从而激活NF-κB p65和IL-10的产生. 针对这种Mct4-NF-κB-IL-10通路可以提供新的结核病治疗方法.
科学领域:
- 免疫学 免疫学 免疫学
- 传染性疾病 传染性疾病
- 细胞生物学 细胞生物学
背景情况:
- 结核病 (TB) 仍然是全球感染性死亡的主要原因.
- 单碳酸盐载体4 (Mct4) 在宿主免疫反应对Mycobacterium tuberculosis (Mtb) 的作用尚不清楚.
- Mct4调节细胞膜间的乳酸运输.
研究的目的:
- 研究Mct4在宿主免疫反应对Mtb感染中的功能.
- 阐明Mct4影响Mtb生存的分子机制.
- 确定结核病治疗的潜在治疗点.
主要方法:
- 在Mtb感染的巨细胞和结核病患者中评估Mct4表达.
- 在巨细胞和小鼠模型中利用Mct4沉默和过度表达.
- 测量了mtb存活率,细胞内乳酸水平,NF-κB p65激活和IL-10的产生.
- 使用IL-10沉默剂,IL-10中和抗体和NF-κB抑制剂 (JSH23).
主要成果:
- 在Mtb感染和结核病患者中,Mct4表达被上调.
- 在体外和体内,Mct4缺乏减少了Mtb的存活率.
- 通过促进乳酸出口,NF-κB p65激活和IL-10产生,Mct4过度表达提高了Mtb的生存率.
- 抑制IL-10或NF-κB信号,取消了Mct4.4对生存的影响.
结论:
- Mct4通过促进细胞内乳酸排放促进Mtb的生存,从而导致NF-κB p65介导的IL-10产生.
- Mct4-NF-κB-IL-10轴代表了对抗结核病的新型治疗标.
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