尼古丁胺对抗人类巨细胞中脂聚糖诱导的低毒细胞信号
Colleen S Curran1, Edward J Dougherty1, Xizhong Cui1
1Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD.
Journal of immunology (Baltimore, Md. : 1950)
|June 14, 2023
概括
尼古丁胺 (NAM) 通过抑制巨细胞激活信号来减少炎症,但可能会损害病原体清除. 这种维生素B3衍生物影响免疫反应,提供潜在的治疗见解.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 像那些含有脂聚糖 (LPS) 的格拉姆阴性细菌一样,会触发巨细胞的免疫反应.
- 由LPS诱导的巨细胞激活促进炎症,细胞和代谢变化.
- 尼古丁胺 (NAM) 是一种维生素B3衍生物,是NAD的前体,对细胞功能至关重要.
研究的目的:
- 研究NAM如何影响巨细胞中LPS诱导的信号通路.
- 了解NAM调节巨细胞激活的分子机制.
主要方法:
- 人类单细胞衍生的巨细胞被用NAM和LPS治疗.
- 分析了翻译后的修改,包括酸化和乙化.
- 评估了蛋白质的无处不在,转录和代谢活性.
主要成果:
- 纳姆抑制了LPS诱导的AKT和FOXO1酸化和p65/RelA乙化.
- NAM促进了p65/RelA和缺氧诱导转录因子-1α (HIF-1α) 的无处不在.
- NAM降低了HIF-1α稳定,糖解,细胞化,NOX2活性和乳酸脱酶A的产生.
结论:
- NAM对抗LPS诱导的巨细胞信号,可能通过增加NAD水平和促进蛋白质体降解.
- NAM可能会减少过度的炎症,但可能会影响病原体清除.
- 对NAM影响的进一步研究对于理解宿主-病原体相互作用和开发干预措施至关重要.
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