由口腔链球菌利用的炎症性巨细胞通过NLRP6炎症酶体增加IL-1B的释放
Sarah Metcalfe1, Michelle Panasiewicz1, Jason G Kay1
1Department of Oral Biology, School of Dental Medicine, University at Buffalo, 3435 Main street, Buffalo, NY 14214, United States.
Journal of leukocyte biology
|July 27, 2023
概括
像Streptococcus gordonii这样的共生细菌可以逃避免疫细胞,促进炎症和互白素-1β释放,从而恶化牙周病. 巨细胞的激活增强了这种细菌的生存和炎症反应.
科学领域:
- 免疫学 免疫学 免疫学
- 微生物学 微生物学
- 口腔健康 口腔健康
背景情况:
- 慢性炎症性牙周病涉及炎症性巨细胞和细胞因子,如介质蛋白 (IL) - 1β.
- 开始性口腔细菌,包括Streptococcus gordonii,对于牙周病的发展至关重要.
- 具有悖论的,炎症性巨细胞增强了被细胞化S. gordonii的生存.
研究的目的:
- 为了研究S. gordonii和激活的巨细胞之间的相互作用.
- 确定巨细胞激活在S. gordonii生存和IL-1β释放中的作用.
- 为了确定由S. gordonii.激活炎症酶的机制.
主要方法:
- 在体外感染巨细胞与活的和死的S. gordonii.
- 测量IL-1β释放的时间.
- 评估不同巨细胞激活状态下的细菌存活率.
- 对炎症组分NLRP6参与的分析.
主要成果:
- 被活体S. gordonii感染的活化巨细胞释放出显著更多的IL-1β.
- 与其他格拉姆阳性微生物相比,S. gordonii的存活更多地依赖于巨细胞激活.
- 由于S. gordonii的炎症酶激活,需要细胞质NLRP6蛋白.
- 在炎症条件下,S. gordonii表现出增强的免疫逃避和炎症媒介释放.
结论:
- 戈尔多尼菌在炎症性巨细胞中逃避免疫破坏,促进IL-1β的释放.
- 巨细胞的激活增强了S. gordonii的生存率及其增加炎症媒介的能力.
- 这些相互作用有助于促进炎症的环境,可能加剧牙周病.
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