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干白素-37通过抑制NLRP3炎症酶激活和调节M1/M2巨细胞极化来改善牙周炎的发展

Liyan Yang¹, Wei Tao¹, Chen Xie²

¹Department of Stomatology, The First Affiliated Hospital of Hainan Medical University, Haikou, China.

Journal of periodontal research

|November 10, 2023

概括

干白素-37 (IL-37) 通过减少炎症和骨质损失,防止牙周炎的进展. 这种抗炎性细胞因子平衡M1/M2巨细胞两极分化,并抑制NLRP3炎症酶激活.

科学领域:

免疫学免疫学免疫学
牙周病学牙周病学
分子生物学分子生物学

背景情况:

牙周炎是一种慢性炎症性疾病,其特征是牙炎症和膜骨损失.
大细胞两极分化在调节牙周炎症方面起着至关重要的作用.
介素-37 (IL-37) 是一种具有已知的免疫调节作用的抗炎细胞因子.

研究的目的:

调查IL-37在调节M1/M2巨细胞极化中的作用,在牙周炎的病原性背景下.
在实验性牙周炎模型中确定IL-37的治疗潜力.

主要方法:

试验室:小鼠巨细胞RAW264.7细胞被IL-37处理,然后被偏向到M1 (LPS诱导) 或M2 (IL-4诱导) 现型. 标记物表达 (iNOS,TNF-α,M1的IL-6,M2的CD206,Arg1,IL-10) 通过RT-qPCR,西部斑点和免疫光检测进行了评估.
在体内:实验性牙周炎被诱导在小鼠使用丝绑定. 用IL-37进行治疗. 使用微型CT和H&E染色评估了膜骨损失. 牙组织分析包括INOS和CD206的免疫组织化学,以及NLRP3炎症组分的西部涂抹.

主要成果:

在实验室中,IL-37治疗使巨细胞偏向M2表型,减少M1标记物和增加M2标记物.
在实验室中,IL-37抑制了NLRP3炎症酶通路 (NLRP3,GSDMD,切割IL-1β,切割caspase-1) 的LPS诱导激活.
在体内,IL-37的使用改善了牙周炎相关的骨再吸收和根损伤. 它在牙组织中降低了M1巨标记物 (iNOS) 和增加了M2标记物 (CD206),同时也抑制了NLRP3炎症酶激活.

结论:

IL-37显示出对牙周炎进展的保护作用.
IL-37通过抑制NLRP3炎症酶激活和重新平衡M1/M2巨细胞极化而起作用.
向IL-37可能是治疗牙周炎的新疗法策略.

关键词:

在IL-37中,它是IL-37.M1/M2巨细胞两极分化在NLRP3炎症酶体中,NLRP3炎症这是一种炎症炎症炎症炎症.牙周炎是指牙周炎的一种疾病.

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