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Porphyromonas gingivalis as a Model Organism for Assessing Interaction of Anaerobic Bacteria with Host Cells

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辅助的指甲子单元和PPAD是必要的TLR2通过Porphyromonas gingivalis的激活

Aleksandra Wielento¹, Grzegorz P Bereta¹, Katarzyna Szczęśniak¹

¹Department of Microbiology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland.

Molecular oral microbiology

|June 22, 2023

概括

Porphyromonas gingivalis 使用基氨酸减弱酶 (PPAD) 来修改膜,然后激活托尔类受体2 (TLR2). 这种相互作用对于触发牙周炎炎炎症反应至关重要.

科学领域:

微生物学微生物学
免疫学免疫学免疫学
口腔生物学口腔生物学

背景情况:

Porphyromonas gingivalis 是一种与牙周炎相关的口腔病原体.
它逃避宿主免疫力,并促进慢性炎症.
像基氨酸减弱酶 (PPAD) 这样的病毒性因素是其致病性的关键.

研究的目的:

调查PPAD和fimbriae在P. gingivalis诱导的主体免疫反应中的作用.
为了确定P. gingivalis如何激活托尔类受体2 (TLR2).
为了确定涉及TLR2激活的特定指部件.

主要方法:

感染野生型和突变P. gingivalis菌株的初级人类牙纤维细胞 (PHGF) 的转录概况.
报告者细胞系测试以评估TLR2连接体活性.
对缺乏PPAD和fimbriae的P. gingivalis菌株的分析.

主要成果:

对于P. gingivalis来说,PPAD和fimbriae对于激活TLR2至关重要.
经PPAD修饰的膜,特别是I型膜,是强大的TLR2激活剂.
通过PPAD修改的辅助指甲子单元 (FimC,FimD,FimE) 作为TLR2连接体起作用.
PHGFs的抗炎激活取决于PPAD和辅助手子子单元.

结论:

通过PPAD修改的辅助指甲子单元对于刺激宿主对P. gingivalis.的反应至关重要.
这种刺激以TLR2依赖的方式发生.
了解这种机制,可以了解牙周炎的病原性.

关键词:

配件膜片子单位配件膜片子单位葡萄牙牙牙病 Porphyromonas gingivalis 这种虫害的素化是指素化.菲姆布里亚 (Fimbriae) 是一座城市.牙纤维细胞牙纤维细胞丁氨酸脱酶是什么?

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