Brief reviewArterial Inflammation and Atherosclerosis
Section snippets
Inflammatory Responses in the Vascular Wall: Infection or Autoimmunity?
A number of potential mechanisms have been implicated in the development of inflammatory reactions in the vascular system. Microbial infection and autoimmune reactions are thought to possess the potential to elicit and maintain vascular inflammation in systemic vasculitides. For example, Wegener granulomatosis has been linked with human parvovirus B19 (Nikkari et al. 1994) and Staphylococcus aureus infection (Stegeman et al. 1994). Likewise, human parvovirus B19 was suggested to be involved in
Impact of Hypercholesterolemia on Vascular Inflammation and General Immune Responsiveness
Hypercholesterolemia is one of the major risk factors in atherosclerosis. Therapeutic intervention using lipid-lowering agents significantly reduces mortality rates in patients with coronary heart disease (Gotto 1998). Interestingly, drugs such as statins also affect general immune responsiveness. For example, statins may act as direct inhibitors of the induction of major histocompatibility complex (MHC)-II expression on endothelial cells by interferon (IFN)-γ thereby suppressing
Linking Immune-Mediated Arterial Inflammation and Cholesterol-Induced Atherosclerosis
In studies on the pathogenesis of pathogen-induced immunopathological disease, it is usually difficult to distinguish between direct pathogen-mediated tissue damage and the immune-mediated inflammatory response. Uncoupling microbial replication and antimicrobial immune responses can be achieved by using mycobacterial heat shock protein (HSP) George et al. 1999, Xu et al. 1992. However, HSP is a rather “general” immune activator that may also induce or aggravate other autoimmune diseases,
Conclusions
In summary, experimental models and many clinical studies have shown that the vascular wall is frequently a target for infectious agents. The scenario of the interplay among infection, autoimmunity, and lipid imbalances and how these factors contribute to the complex pathogenesis of atherosclerosis is depicted in Figure 1. Hypercholesterolemia, genetic susceptibility, and autoimmune diseases may alter general immune reactivity and thereby enhance the susceptibility of the arterial wall to
Acknowledgements
The authors thank Dr. Kathy McCoy for critical reading of the manuscript. This work was supported by the Swiss National Science Foundation and the Kanton Zürich.
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