病原微生物感染所致炎症反应在动脉粥样硬化（AS）中的作用日益受到重视，我们前期证实病原微生物感染的颈动脉粥样硬化狭窄患者血清炎症因子YKL-40明显增高，且与斑块不稳定性有关，其机制目前尚不甚清楚。我们发现巨细胞病毒（CMV）感染血管内皮细胞（EC）后可分泌携载miRNAs的exosome；将exosome与血管平滑肌细胞（SMC）共培养，其可转运至SMC，并促进SMC增殖和YKL-40表达。据此提出假说：CMV感染EC可分泌携载功能性组分如miRNA的exosome与SMC发生通讯作用，其可能通过调控YKL-40介导AS的炎症机制，影响AS的发生发展。本项目拟进一步筛选CMV感染EC来源exosome特异性miRNAs，明确其在EC/SMC间的通讯作用及对YKL-40的调控机制，进而探讨它们在AS发生发展过程中的作用，为AS发病机制研究提供新思路，甚至提供可能的生物标记物及干预靶点。

The role of chronic inflammation of pathogen infection in atherosclerosis(AS) gain more and more attention recent years. Our study showed that plasma YKL-40 increased in the patients with carotid atherosclerotic stenosis(CAS) with pathogen infection compared with those without infection. Futher study indicated that YKL-40 increased the plaque instability，but its mechanism isn’t completely clear till now. We fould that vascular endothelial cell (EC)infected by cytomegalovirus(CMV) could secret exosome carried with miRNAs. When exosome was co-cultured with smooth muscle cell(SMC), the exosome could transfer to SMC and promote SMC proliferation，and YKL-40 expression in SMC was also increased. According to the results,we hypothesize that CMV-infected EC secrets exosome carried with miRNAs, which can communicate with SMC through regulating YKL-40 and then play an important role on the pathogenesis of AS. Therefore in this program, we plan to screen the specific miRNAs of exosome derived from CMV-infected EC, and investigate the role and mechanism of exosome derived-miRNAs and YKL-40 on the communication between EC and SMC as well as their role on the pathogenesis of AS. The results of this program will help give further new insights into the role of inflammation on AS and provide new possible target moleculars for early prevention and treatment for AS.