Persistent bacterial infection and vascular disease
Autoimmune reaction to infection could be an important factor in atherogenesis.
By (email@example.com) | August 25, 2000
LONDON, August 25 (SPIS MedWire). A new study reported in Circulation offers strong evidence that persistent bacterial infection is associated with atherosclerosis, and that heat shock protein 60 (HSP60) antibodies may mediate the relationship. Mayr and colleagues at the University of Innsbruck Medical School, Austria, analyzed data from the Bruneck Study — a large population-based study that randomly sampled all inhabitants of Bruneck aged between 40 and 79. A total of 826 subjects were included in the analysis, which involved clinical examination with cardiological and neurological priority. Anti-C pneumoniae IgA antibodies were associated with the prevalence of atherosclerosis in carotid and femoral arteries (p=0.011 and p=0.035, respectively) and this relationship remained significant after adjustment for multiple risk factors. Anti-H pylori IgG antibodies correlated significantly with carotid atherosclerosis, but only in patients of low social status, and there was no correlation with atherosclerosis in the femoral arteries. Elevated antibodies to CMV were not associated with atherosclerotic lesions in either site. C. pneumoniae was also shown to be a significant predictor of intima-media thickness, which is a well-established precursor of atherosclerosis. Notably, none of the findings were substantially altered when the analysis was restricted to non-smokers. Taken together, the authors say their findings "suggest that immune reactions to mycobacterial heat shock protein 65 are linked with bacterial but not viral infections." Although the mechanism by which infections are involved in vascular disease remains to be elucidated, Mayr et al suggest that an abundance of bacterial HSP60 may evoke an autoimmune response in susceptible individuals because of its high homology with the human homologue, which in turn mediate vascular cytotoxicity on stressed endothelial cells.