Dissemination of Chlamydia pneumoniae to the vessel wall in atherosclerosis.

Heart disease and stroke are the result of atherosclerotic vascular lesions. It is becoming increasingly clear that an infection may be an important initiating component within the atherogenic process. However, in order for the infection to contribute to atherosclerosis, it must first be capable of disseminating to the vessel wall. Chlamydia pneumoniae is an example of an infectious atherogenic stimulus. The present treatise reviews our knowledge concerning dissemination of infectious agents like C. pneumoniae. Three factors can be identified that modulate the severity of the infection in the vascular wall. First, although all vascular cell types appear to be infected with agents like C. pneumoniae, there are differences in the sensitivity to infection amongst these cell types. Second, the lipid environment is important in defining the effects of C. pneumoniae on atherosclerotic disease. Third, the inflammatory/atherosclerotic interaction is influenced by the specific infectious stimuli employed. The in situ atherogenic effects of C. pneumoniae may be specific to this organism and may not occur with related infectious agents like C. trachomatis. Despite the identification of these three factors, controversy exists surrounding specific characteristics of these effects. This may be the result of a plethora of differing experimental conditions (different labs, different lipids, different cell types or lines, and different C. pneumoniae characteristics (infection, dosage, duration, etc.)). Further study of these important phenomena is clearly warranted in view of the potential importance of infection to the atherosclerotic disease.