Role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 6 in activation of inflammation in human umbilical vein endothelial cells stimulated by Porphyromonas gingivalis-an in vitro study.
Role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 6 in activation of inflammation in human umbilical vein endothelial cells stimulated by Porphyromonas gingivalis-an in vitro study.
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DOI：
10.1016/j.jds.2022.09.009
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发表时间：
2022-09
影响因子：
3.5
通讯作者：
X. Lou;Jian-ru Liu;X. Ouyang;Wenyi Liu;Ying Xie;Jinsheng Zhong;Peiying Lv;Shengnan Zhang
中科院分区：
文献类型：
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作者：
X. Lou;Jian-ru Liu;X. Ouyang;Wenyi Liu;Ying Xie;Jinsheng Zhong;Peiying Lv;Shengnan Zhang
背景/目的牙龈卟啉单胞菌（porphyromonas gingivalis）可诱导血管内皮细胞活化，促进动脉粥样硬化的形成。核苷酸结合寡聚化结构域样受体家族含pyrin结构域（NLRP） 6可以识别ep。但其在动脉粥样硬化中的作用尚不清楚。本研究旨在探讨NLRP6在p刺激的人脐静脉内皮细胞（HUVECs）炎症激活中的作用。gingivalis。材料与方法NLRP6在含p和不含p的HUVECs中的表达水平。观察牙龈损伤。下调NLRP6在HUVECs中的表达，检测白细胞介素(IL)-1β、IL-6、IL-8、肿瘤坏死因子-α (TNF-α)和单核细胞趋化蛋白(MCP)-1的表达水平。然后，用p刺激nlrp6过表达的HUVECs。并与p触发的HUVECs进行比较。gingivalisonly。为了评估NLRP6对细菌免疫逃逸的影响，我们将NLRP6过表达，p。计算huvec中存活的牙龈病。结果snlrp6在HUVECs中表达，p后表达量减少。gingivalisstimulation。下调NLRP6可降低huvec中IL-1β、IL-6、IL-8、TNF-α和MCP-1的表达水平。这些细胞因子在nlrp6过表达的huvec与p。与p细胞组相比，p细胞组的牙龈刺激明显增加。gingivalis-stimulation。此外，NLRP6的过表达减少了p的菌落。牙龈病在HUVECs中的存活。结论nlrp6调节p引起的HUVECs炎症的激活。牙龈在p中起着重要作用。牙龈内皮细胞存活。
Background/purposePorphyromonas gingivalis (P. gingivalis) could induce the activation of vascular endothelial cells and promote the formation of atherosclerosis. Nucleotide-binding oligomerization domain-like receptor family pyrin domain containing (NLRP) 6 could recognizeP. gingivalis,but its role in atherosclerosis was unknown. The purpose of this study is to investigate the role of NLRP6 in the activation of inflammation in human umbilical vein endothelial cells (HUVECs) stimulated byP. gingivalis.Materials and methodsThe expression level of NLRP6 in HUVECs with or withoutP. gingivalis-challenge was observed. Down-regulating the expression of NLRP6 in HUVECs, the expression levels of interleukin (IL)-1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein (MCP)-1 were detected. Then, the HUVECs with NLRP6-overexpressed were stimulated byP. gingivalis, the levels of inflammatory cytokines above were examined and compared with those in HUVECs triggered byP. gingivalisonly. To evaluate the effect of NLRP6 on bacterial immune escape, the NLRP6 was overexpressed, and the colonies ofP. gingivalisthat survived in HUVECs were calculated.ResultsNLRP6 was expressed in HUVECs and decreased afterP. gingivalisstimulation. Downregulation of NLRP6 decreased the expression levels of IL-1β, IL-6, IL-8, TNF-α and MCP-1 in HUVECs. Those cytokines above in NLRP6-overexpressed HUVECs withP. gingivalis-stimulation significantly increased than in the cells withP. gingivalis-stimulation only. Furthermore, over-expression of NLRP6 decreased the colonies ofP. gingivalissurvival in HUVECs.ConclusionNLRP6 regulated the activation of inflammation in HUVECs triggered byP. gingivalisand played an important role inP. gingivalissurvival in endothelial cells.