DOCK8通过调节有氧糖溶解来抑制败血症中中性粒细胞的免疫功能
Hongjun Zhu1, Junlong Xu2, Ke Li2
1Clinical Laboratory, The Sixth Affiliated Hospital of Wenzhou Medical University, Lishui People's Hospital, Lishui City, China.
Immunity, inflammation and disease
|August 30, 2023
概括
缺少DOCK8 (细胞动力学指标8) 蛋白质会在败血症期间损害中性粒细胞的免疫功能. 低水平的DOCK8促进炎症并改变细胞代谢,这表明DOCK8是潜在的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 细胞的新陈代谢
背景情况:
- 败血症会触发复杂的免疫反应,通常涉及中性粒细胞功能障碍.
- 在败血症诱导的免疫调节中,DOCK8 (细胞动化8的分离器) 的作用尚不清楚.
研究的目的:
- 为了研究DOCK8在败血症中的功能.
- 探索DOCK8,中性粒细胞功能和毒症中的有氧糖解之间的关系.
主要方法:
- 在败血症患者中对DOCK8表达和通路的生物信息分析.
- 使用脂多糖刺激的败血症小鼠模型和细胞模型.
- 检测DOCK8表达,细胞活力,炎症性细胞因子 (TNF-α,IL-1β,IL-6),中性粒细胞化学反应,细胞和细胞糖解 (ECAR,酸盐,乳酸盐,ATP).
主要成果:
- 在败血症患者和中性粒细胞中,DOCK8的表达下调.
- 低DOCK8表达与增加的有氧糖解,增强的中性粒细胞增殖,化学毒性,细胞化和炎症性细胞因子水平的升高相关.
- DOCK8的下调促进了与糖解相关的蛋白质表达 (HK-2,PKM2,LDHA) 和增加了糖解代谢物.
结论:
- 通过调节有氧糖解,DOCK8在败血症诱导的中性粒细胞免疫功能中起着抑制作用.
- 准DOCK8可能提供一种治疗策略,以减轻败血症引起的炎症和免疫功能障碍.
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