Aim To investigate the roles of N-WASP in angiogenesis induced by Chlamydia pneumoniae (C.pneumoniae) infection and its possible mechanism. Methods After proliferation culture, C.pneumoniae infected human vascular endothelial cell (VEC), and immunofluorescence staining confirmed successful infection. The phosphorylation level of N-WASP was detected by Western blot in VEC infected by C.pneumoniae. The effect of N-WASP specific inhibitor Wiskostain on VEC viability was detected by CCK-8. The effect of Wiskostain working concentrations on C.pneumoniae infection rate was detected by immunofluorescence assay. After C.pneumoniae infected VEC with 5 μmol/L Wiskostain pretreatment, capillary tube formation assay was performed to observe the changes of VEC angiogenesis ability. Results Under fluorescence microscope, typical C.pneumoniae inclusions were found in infected VEC cytoplasm. After VEC was infected with C.pneumoniae for 10 and 24 hours, the level of N-WASP phosphorylation was significantly higher than that in the control group. Capillary tube formation assay showed that after VEC was infected with C.pneumoniae for 16 hours, the number of capillary tube node was significantly higher than that in the control group (P＜0.05). After the pretreatment of VECs with Wiskostain, the role of C.pneumoniae infection in promoting the formation of capillary tube node was significantly weakened, and it was almost impossible to form capillary tube structure (P＜0.05). Conclusion C.pneumoniae infection may promote the formation of new blood vessels possibly through N-WASP.