Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China.
Institute of Infectious Disease, School of Medicine, Xiamen University, Xiamen, China.
Front Cell Infect Microbiol. 2019 Jun 21;9:220. doi: 10.3389/fcimb.2019.00220. eCollection 2019.
The pathological features of syphilis, a disease caused by (), are characterized by vascular involvement with endarteritis and periarteritis. Little is known about the interactions of infiltrating immunocytes with human dermal vascular smooth muscle cells (HDVSMCs) in arterioles during the immunopathogenesis of syphilis. In the present study, we demonstrated that stimulation of HDVSMCs with resulted in the upregulated gene transcription and protein expression of interleukin (IL)-6, monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule-1 (ICAM-1) in a dose- and time-dependent manner. Moreover, the migration and adhesion of THP-1 cells to HDVSMCs were significantly suppressed by anti-MCP-1 and anti-ICAM-1 neutralizing antibodies, respectively. Further studies revealed that activated the NF-κB signaling pathway in HDVSMCs. Inhibition of NF-κB suppressed -induced IL-6, MCP-1, and ICAM-1 expression. In addition, the migration and adhesion of THP-1 cells to -treated HDVSMCs were significantly decreased by pretreatment with an NF-κB inhibitor. These findings demonstrate that induces the production of IL-6, MCP-1, and ICAM-1 in HDVSMCs and promotes the adherence and migration of THP-1 cells to HDVSMCs through the NF-κB signaling pathway, which may provide new insight into the pathogenesis of infection.
梅毒是由 （）引起的疾病，其病理学特征是血管受累伴动脉炎和动脉周围炎。在梅毒的免疫发病机制中，浸润免疫细胞与人类真皮血管平滑肌细胞（HDVSMCs）在小动脉中的相互作用知之甚少。在本研究中，我们证明了 刺激 HDVSMCs 会导致白细胞介素（IL）-6、单核细胞趋化蛋白-1（MCP-1）和细胞间黏附分子-1（ICAM-1）的基因转录和蛋白表达在剂量和时间上呈依赖性上调。此外，抗 MCP-1 和抗 ICAM-1 中和抗体分别显著抑制 THP-1 细胞向 HDVSMCs 的迁移和黏附。进一步的研究表明， 激活了 HDVSMCs 中的 NF-κB 信号通路。NF-κB 抑制可抑制 - 诱导的 IL-6、MCP-1 和 ICAM-1 表达。此外，NF-κB 抑制剂预处理可显著降低 - 处理的 HDVSMCs 中 THP-1 细胞的迁移和黏附。这些发现表明， 通过 NF-κB 信号通路诱导 HDVSMCs 中产生 IL-6、MCP-1 和 ICAM-1，并促进 THP-1 细胞向 HDVSMCs 的黏附和迁移，这可能为 感染的发病机制提供新的见解。
