AimTo investigate the role of PI3K/Akt in vascular smooth muscle cell (VSMC) migration induced by Chlamydia pneumoniae (C.pn) infection.MethodsThe successful infection of rat VSMCs with C.pn was identified by transmission electron microscope; After VSMCs were pretreated with the specific PI3K inhibitor LY294002, wound-healing assay and Transwell assay were performed to observe the changes in the migration ability of VSMCs；The phosphorylation level of Akt was detected by Western blot.ResultsThe typical C.pn elementary bodies were observed in the infected VSMCs under the transmission electron microscope; The migration ability of VSMCs infected with C.pn was enhanced and significantly higher than that of control group at 24 h postinfection in the cell migration assay (p<0.05); Western blot results showed that the phosphorylation level of Akt was up-regulated and also higher than that of control group at 24 h after infection（p<0.05）.The effects of C.pn infection on the VSMC migration and the phosphorylation level of Akt in the VSMCs were significantly inhibited by the specific PI3K inhibitor LY294002.ConclusionC.pn infection may promote VSMC migration via activation of PI3K/Akt.