Infections, heat shock proteins, and atherosclerosis

Recent evidence indicates that infections or a pathogen burden contribute to the development and progression of atherosclerosis. While the mechanism of infection contributing to the pathogenesis is not fully elucidated, I hypothesize that heat shock proteins may be a link between infections and atherosclerosis. Heat shock proteins are a highly conserved family of proteins expressed in most cell types and have been shown to play a general role in protecting cells in response to stress. It has been demonstrated that Chlamydia and human HSP60 coexist in atherosclerotic lesions. Bacterial and human heat shock proteins have been found in soluble form in the general circulation of patients with atherosclerosis. Both heat shock proteins can stimulate cells to express adhesion molecules and proinflammatory cytokines. Certain organisms synthesize heat shock proteins that have close structural homology with human heat shock proteins. Because of the immunologic molecular mimicry between bacterial and human HSP60, it could be an autoantigen involved in eliciting cell-mediated and humoral immune responses that cause vessel injury leading to atherosclerosis. The aim of this review is to provide an update overview on the involvement of heat shock proteins in the pathogenesis of atherosclerosis in response to infections.