巨细胞偏向于亲炎性表型,并延迟中性粒细胞效细胞化,以增强聚聚菌的JP2清除能力
Koren Hashai1,2, Fairuz Abadi1,2, Dana Clyman1,2
1Faculty of Dental Medicine, The Hebrew University, Jerusalem, Israel.
Journal of periodontal research
|July 14, 2023
概括
在Aggregatibacter actinomycetemcomitance (JP2) 感染期间,巨细胞延迟了中性粒细胞细胞分裂,促进了细菌清除,但可能会增加牙周组织损伤. 这种中性粒细胞-巨细胞交叉对话是理解牙周炎炎炎症解决的关键.
科学领域:
- 在牙周病的背景下研究免疫细胞之间的复杂相互作用.
- 专注于中性粒细胞和巨细胞在感染聚聚细菌 (JP2) 时的相互作用.
背景情况:
- 牙切口模式牙周炎 (MIPP) 是由下细菌发起的,未解决的宿主反应有助于组织破坏.
- 中性粒细胞与MIPP的发病有关,但在炎症解决过程中由巨细胞清除它们的清除程度尚不清楚.
研究的目的:
- 在JP2感染期间检查中性粒细胞-巨细胞交叉交谈.
- 在此背景下,确定参与炎症解消和细胞分裂的因素.
主要方法:
- 利用了暴露于JP2的人类分化的中性粒细胞和巨细胞 (分别来自HL60和THP1细胞).
- 测量了反应性氧物种 (ROS),CD47表达,细胞活力,巨细胞极化 (CD163,CD68),细胞因子分泌 (TNFα,IL-10),以及血细胞分裂.
- 在C57Bl/6小鼠的体内模型中使用,包括巨细胞枯竭和中性粒细胞CD47水平的评估.
主要成果:
- JP2感染增加了细胞外ROS. 巨细胞通过抑制CD47下降表达,表现出M1极化和延长中性粒细胞的存活率.
- 巨细胞在JP2感染期间延迟了中性粒细胞细胞分裂,增强了细菌清除,但可能会导致炎症.
- 在小鼠中的巨细胞枯竭减少了细菌清除和中性粒细胞CD47的减少,反映了体外发现.
结论:
- 在JP2感染期间降低中性粒细胞效细胞化可能会促进细菌清除.
- 这一过程可能会导致炎症介导的牙周组织损伤,突出显示MIPP病变的关键方面.
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