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Updated: Apr 12, 2026

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Infection and Atherosclerosis Development
Lee Ann Campbell1, Michael E Rosenfeld2
1Department of Epidemiology, School of Public Health, Seattle, Washington, USA.
Insights
Infectious agents, including bacteria and viruses, may play a role in atherosclerosis development by triggering inflammation and vascular cell dysfunction. Proving a direct link in humans remains challenging despite animal model evidence.
Area of Science:
- Cardiovascular Science
- Infectious Disease Immunology
Background:
- Atherosclerosis is a chronic inflammatory vascular disease characterized by lipid accumulation.
- While lipid deposition is a known factor, infectious agents are increasingly implicated in its pathogenesis.
- Infections may directly affect vascular cells or indirectly induce inflammatory responses.
Purpose of the Study:
- To review infectious agents linked to atherosclerosis.
- To focus on agents with demonstrated biological plausibility in animal models.
- To discuss challenges in establishing a causal role in human disease.
Main Methods:
- Review of seroepidemiological studies.
- Identification of infectious agents in human atherosclerotic tissue.
- Analysis of experimental studies in animal models of atherosclerosis.
Main Results:
- Multiple bacterial and viral pathogens have been associated with atherosclerosis.
- Animal models show infection can accelerate atherosclerotic processes.
- Biological plausibility for certain agents is supported by experimental data.
Conclusions:
- Infectious agents are potential contributors to atherosclerosis through direct or indirect mechanisms.
- Evidence from animal models supports a role for specific pathogens.
- Further research is needed to overcome challenges in proving infection's role in human atherosclerosis.
Abstract:
Atherosclerosis is a chronic disease hallmarked by chronic inflammation, endothelial dysfunction and lipid accumulation in the vasculature. Although lipid modification and deposition are thought to be a major source of the continuous inflammatory stimulus, a large body of evidence suggests that infectious agents may contribute to atherosclerotic processes. This could occur by either direct effects through infection of vascular cells and/or through indirect effects by induction of cytokine and acute phase reactant proteins by infection at other sites. Multiple bacterial and viral pathogens have been associated with atherosclerosis by seroepidemiological studies, identification of the infectious agent in human atherosclerotic tissue, and experimental studies demonstrating an acceleration of atherosclerosis following infection in animal models of atherosclerosis. This review will focus on those infectious agents for which biological plausibility has been demonstrated in animal models and on the challenges of proving a role of infection in human atherosclerotic disease.
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