The concept that atherosclerosis was induced by environmental factors such as smoking and high fat intake was perturbated when inflammation was found to be prominent in atherosclerotic lesions. Chlamydophila pneumoniae but also other microbes inducing chronic endothelial infections have been implicated, particularly cytomegalovirus (CMV) and the gastric pathogen Helicobacter pylori. Large sero-epidemiological studies in different parts of the world have shown seroconversion to C. pneumoniae in patients with myocardial infarction, stroke and other forms of cardiovascular disease. The seroprevalence rates vary between 50 and 75%. Older individuals show higher seropositivity rates, suggesting that re-infection may be common. Using polymerase chain reaction (PCR) and immunohistochemistry, several studies have shown C. pneumoniae DNA in atherosclerotic lesions but not in normal vessels, although other studies have failed. Animal models with C. pneumoniae inducing atherosclerotic lesions have been established. The chlamydia LPS induces foam cell formation of monocytes, and the heat shock protein (Hsp) 60 oxidises low-density lipoproteins. Hsp 60 causes transcription of NF-κB and initiates deleterious immune response. Hsp 60, cross-reacting with human Hsp60, may also be involved in molecular mimicry which is part of the chronicity of C. pneumoniae infection. A peptide produced by C. pneumoniae mimics human heart muscle protein, which causes immune sentries. A co-infection of C. pneumoniae with H. pylori increased expression of vascular cell adhesion molecules (VCAM-1) in ApoE knockout mice, which may enhance atherogenesis.