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牙周炎中中性粒细胞外陷水平升高:对牙周上皮质上皮质的角质化和屏障功能的影响

Ya-Yun Cui¹, Yi-Heng Yang², Jia-Yi Zheng²

¹Shanghai Engineering Research Center of Tooth Restoration and Regeneration & Tongji Research Institute of Stomatology & Department of Periodontology, Stomatological Hospital and Dental School, Tongji University, Shanghai, China.

Journal of clinical periodontology

|June 5, 2024

概括

中性细胞细胞外陷 (NETs) 在牙周炎中升高,通过ERK/KLF4通路损害牙角质细胞屏障功能和角质化,表明新的治疗点.

科学领域:

口服免疫学口服免疫学
牙周病机制牙周病的机制
皮质生物学皮质生物学

背景情况:

牙周炎与牙屏障功能受损有关.
中性粒细胞外细胞陷 (NETs) 在炎症和组织损伤中发挥作用.
NETs对牙角质化和屏障完整性的特定影响尚未完全理解.

研究的目的:

在牙周炎患者中量化NET水平.
研究NETs对人类牙角质细胞 (HGKs) 角质化和屏障功能的影响.
阐明在HGKs中NET诱导的变化背后的分子机制.

主要方法:

收集了牙周炎患者和健康对照者的唾液,牙裂液 (GCF) 和牙组织.
在各种生物样本中测量了NET水平.
用NET刺激HGKs并分析了角质化标记物,屏障功能指标,细胞内和上皮质透性.
研究了ERK/KLF4信号通路的参与.

主要成果:

与对照组相比,牙周炎患者的NET水平显著更高.
在HGKs中,NET刺激降低了角质化标记物 (involucrin,cytokeratin 10) 和屏障蛋白 (zonula occludens 1,E-cadherin) 的表达.
NETs导致细胞内的减少,并增加了上皮质屏障的透性.
NET诱导的角质化抑制依赖于ERK/KLF4通路.

结论:

NETs显著增加牙周炎,导致牙屏障功能受损.
NETs通过ERK/KLF4信号轴抑制角质化并破坏HGK中的上皮屏障.
针对NET或ERK/KLF4通路可能为牙周炎相关的牙角质化缺陷提供治疗策略.

关键词:

表面上皮质屏障的一个障碍.人类牙角质细胞质化 (keratinization) 是一种质化过程.中性粒细胞外细胞陷牙周炎是指牙周炎的一种疾病.

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