Background Coronary artery disease(CAD) is a major cause of mortality throughout the world. The pathogenesis of CAD is based on the process of atherosclerosis. The accepted risk factors linked to CAD indued dyslipidemia, smoking, hypertension, diabetes, age, gender, and family history. However, these risk factors have been estimated to account for only about one-half of the incident of CAD. Recently, It is thought that the infection of some viral and bacteria agents (such as chlamydia pneumoniae, herpes viruses, cytomegalovirus) may associationed with atherosclerosis .Chlamydia pneumoniae(C.pneumoniae)is a common cause of acute respiratory conditions, such as pneumoniae, sinusiitis, bronchitisand pharyngitis. In an/interrnational study, an average of about 50% of adults were found to have antibodies to C.pneumoniae. Recently, chronic C.pneumoniae infection has been suggested as a trigger and promoter of atherosclerosis and acute coronary artery disease. But further and more studies should be made to confirm the theory. Several groups have demostrated the ability of C.pneumoniae to infect andreplicate in cell types found within the atherosclerotic lesion, including endothelial cells, smooth muscle cells, and macrophages, that provide the possible to study the relation of C.pneumoniae and atherosclerotisis in detail.Vascular local inflammation response indused the rolling ^ adhesion and migration of circulating polymorphonuclear leukocytes (PMN) to and under vascular endothelial cells, that make an. important role in the trigger of atherosclerosis and the accure of acute coronary artery disease. Intercellular adhesion molecule 1 (ICAM-1) and vascular adhesion molecule 1(VCAM-1) are the major adhesion molecule expression on the surface of vascular endothelial cells to mediate the interaction between monocytes and endothelial cells that belong to immunoglobulin superfamily. Increased expression of ICAM-1 and VCAM-1 have been frequently found in atherosclerotic lesions.Objective The present study investigated the effects of C.pneumoniae infection on the expression of ICAM-1 and VCAM-1 in cultured human Umbilical Vein Endothelial Cells .Methods After propagated in HEP-2 cells, C.pneumoniae organisms ( strain AR-39 ) were infected human umbilical vein endothelial cells( HUVECs), we assessed the infection by ectromicroscope and polymerase chain reaction(PCR). The expression of ICAM-1 and VCAM-1 on HUVECs were detected by flow cytlemetry before infection and 12h> 24h. 48h* 72h after the infection. RT-PCR was used to detect the ICAM-1 and VCAM-1 mRNA expression. Results1<. C.pneumoniae nucleonic acids were detected in HUVECS after infection by PCR. Observed by electmicroscope, we found elementany body( EB), reticulate body(RB), and inclusion body( IB ) in HUVECs. It showed that C.pneumoniae was able to infect and live hi cultured HUVECs.2, The result of FCM showed that there were expression of 1C AM-1 and VCAM-1 on the surface of cultured HUVECs. At the time of at 12h to 72h after C.pneumoniae infection, ICAM-1 average expression rates were higher than that of Oh (88.7%, 98.1%, 95.4%, 91.3% VS 74.6% , PO.01 ), the peak was at the time of 24h after infection ; The total expression levels were also higher than that of Oh (3.83?.37, 8.96?.85, 10.15?.09, 5.75?.53 VS 2.87?.84, P<0.01), the peak was at the time of 48h after infection. At the time of at 24h to 72h after infection, ICAM-1 average expression levels were higher than that of Oh(9.17?.90, 10.60?.78, 6.29?.46 VS 3.84?.02, P<0.01), there were no significant decrease at the tune of 12h after infection (4.31?.36 VS 3.84?.02, P>0.05).At the time of at 12h to 72h after infection, VCAM-1 average expression rates were higher than that of Oh (3.53%, 20.76%, 10.6%, 8.51% VS 1.27%, P<0.01 ), the peak was at the time of 24h after infection ; The total expression levels were also higher than that of Oh (0.091?.068, 0.333?.150, 0.135?.045, 0.167?.080 VS 0.017?.006, P<0.05^ the peak was about at the time of 24h after infection. At th