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在慢性牙牙周炎中,P.Gingivalis通过调节肝素表达来诱导巨细胞的两极分化

Jinge Dou¹, Xuan Chen², Jinglan Zhang¹

¹State Key Laboratory of Oral Diseases & National Center for Stomatology & National Clinical Research Center for Oral Diseases & Department of Operative Dentistry and Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, Sichuan, China.

International immunopharmacology

|September 15, 2024

概括

在慢性上牙周炎 (CAP) 中,肝素 (一种关键的铁调节剂) 通过IL-6/STAT3通路促进M1巨细胞的两极分化,导致骨组织损伤. 这突出了hepcidin 的作用.

科学领域:

免疫学免疫学免疫学
口腔生物学口腔生物学
铁的新陈代谢铁的新陈代谢

背景情况:

肝素调节铁代谢,并通过IL-6/STAT3信号在炎症条件上升调节.
Porphyromonas gingivalis (P. gingivalis) 和其脂多糖 (LPS) 涉及慢性牙周炎 (CAP) 的病原性.
了解肝素在P. gingivalis引起的骨损伤中的作用对于CAP管理至关重要.

研究的目的:

调查肝素在P. gingivalis诱导的骨组织损伤中的作用和机制.
为了确定肝素是否通过CAP中的IL-6/STAT3信号通路促进巨细胞M1极化.

主要方法:

来自GEO数据库的GSE77459数据集的分析,用于炎症性牙纸组织中的肝素表达.
用RT-qPCR和免疫光染色检测人类CAP组织中的肝素表达和巨相关性.
在实验室研究中,使用小鼠骨髓衍生巨细胞 (BMDMs),用P. gingivalis LPS刺激,用IL-6/STAT3抑制剂治疗 (统计).

主要成果:

肝素表达通过人类CAP组织的IL-6/STAT3信号调节,并与巨细胞两极分化相关.
编码肝素的基因高度表达,并且与CAP组织中的M1巨有关.
P. gingivalis LPS通过IL-6/STAT3通路在巨细胞中诱导了hepcidin表达和M1极化;Stattic抑制了这些效应.

结论:

CAP中的巨细胞表现出高水平的肝素表达,导致巨细胞代谢变化和M1极化.
赫普西丁在P. gingivalis诱导的骨组织破坏中起着重要作用.

关键词:

慢性上性牙周炎慢性牙周炎肝素是一种肝素.豁免权是一种豁免权.炎症炎症是一种炎症.巨细胞是一个巨细胞.

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