Recent evidence suggests that common chronic infections may contribute to the initiation and/or progression of atherosclerosis. Infection of the vascular wall with Chlamydia pneumoniae, a gramnegative bacterium, has been linked with coronary heart disease, myocardial infarction and stroke in epidemiological studies and in pathological studies using immunohistochemistry and electron microscopy. In addition striking evidence for an active role of Chlamydia pneumoniae in atherogenesis has been provided in animal models and from preliminary data of intervention trials. Although these observations strongly indicate an involvement of Chlamydia pneumoniae in the pathogenesis of atherosclerosis, a causal relationship has not been established yet. In the last years several interesting papers have dealt with the molecular mechanisms how an infection with Chlamydia pneumoniae affects the vascular wall to initiate or facilitate vascular dysfunction.