Infectious Agents and Atherosclerosis Pathogenesis
Summary
Atherosclerosis is now recognised as a chronic inflammatory condition of the arterial wall in which infectious agents act as co-factors that accelerate lesion initiation and progression. Bacteria such as Chlamydia pneumoniae and Helicobacter cinaedi, and viruses including cytomegalovirus and herpes simplex virus, can infect endothelial cells, smooth muscle cells and macrophages, triggering oxidative stress, immune cell recruitment and foam cell formation. Pathogen-derived molecular patterns engage innate receptors, leading to cytokine and reactive oxygen species production, endothelial dysfunction and lipid oxidation. Persistent or latent infections sustain a low-grade inflammatory milieu, promoting plaque growth and destabilisation. Understanding these microbe-host interactions has global significance for cardiovascular risk stratification and may yield novel antimicrobial or immunomodulatory therapies to complement lipid-lowering and anti-thrombotic strategies.
Research from Nature Portfolio
Investigations into Helicobacter cinaedi have identified a specific bacterial protein, termed Cinaedi Atherosclerosis Inflammatory Protein (CAIP), that is recognised by T cells within human atheromatous plaques. CAIP-specific T cells display a type 1 helper (Th1) profile and secrete interferon-γ, driving macrophage differentiation towards a pro-inflammatory state. Exposure of human macrophages to recombinant CAIP promotes foam cell formation by enhancing lipid uptake and sustaining inflammatory gene expression, indicating that eradication of H. cinaedi or blockade of CAIP–macrophage interactions could lessen plaque inflammation and reduce cardiovascular events.
Infectious Agents and Atherosclerosis Pathogenesis publication trend
The graph below shows the total number of articles in infectious agents and atherosclerosis pathogenesis across all publications each year (not limited to Nature Index journals).
Technical terms
Foam cell: A macrophage engorged with oxidised lipids, central to early plaque formation.
Pyroptosis: A pro-inflammatory form of programmed cell death mediated by gasdermin-dependent pore formation.
Pathogen-associated molecular patterns (PAMPs): Conserved microbial molecules detected by innate immune receptors.
NLRP3 inflammasome: A cytosolic multiprotein complex that activates inflammatory caspases and interleukin-1β release.
Th1 response: A type of adaptive immunity driven by interferon-γ-producing T helper cells, promoting macrophage activation.
References
- Virus-Associated CD8+ T-Cells Are Not Activated Through Antigen-Mediated Interaction Inside Atherosclerotic Lesions. Arteriosclerosis Thrombosis and Vascular Biology (2024).
- Hypotheses on Atherogenesis Triggering: Does the Infectious Nature of Atherosclerosis Development Have a Substruction?. Cells (2023).
- HCMV-IE2 promotes atherosclerosis by inhibiting vascular smooth muscle cells’ pyroptosis. Frontiers in Microbiology (2023).
- Infectious Agents in Atherosclerotic Cardiovascular Diseases through Oxidative Stress. International Journal of Molecular Sciences (2017).
- The Helicobacter cinaedi antigen CAIP participates in atherosclerotic inflammation by promoting the differentiation of macrophages in foam cells. Scientific Reports (2017).
About these summaries
This Nature Research Intelligence Topic summary is created with the cited references and a large language model. We take care to ground generated text with facts, and have systems in place to gain human feedback on the overall quality of the process in line with our AI principles. We strive to create accurate and useful summaries for people unfamiliar with the research topic and that supports this goal. These pages are a beta release and will be updated as we learn how best to help people gain value from a research topic summary.
Turn complex research questions into confident strategic decisions
When you're under pressure to set direction, justify investment, or understand your competitive position, you need more than raw data — you need trusted insights you can act on.
Benchmark your performance against global peers using robust, methodologically sound analysis.
Combine quantitative metrics with qualitative expert insight to uncover strengths, gaps and emerging opportunities.
Gain tailored, decision-ready recommendations aligned to your strategic priorities.
Talk to us to learn more about our data dashboards and bespoke strategy reports.
Grow research skills, confidence and careers with training built for every stage of the research lifecycle.
Developed with Nature Portfolio journal Editors and internationally renowned experts. Discover three ways to learn:
Self-paced, online courses in convenient bite-sized units, covering key skills across scientific writing, publishing, grant writing, data analysis, and more.
Expert trainer-led workshops with hands-on exercises and real-time feedback across core research skills, delivered via interactive group sessions.
Editor-led workshops combining core principles in writing and publishing, personalised 1:1 feedback from Nature Portfolio Editors and hands-on exercises.
Explore course catalogues and workshop agendas, enquire about the options or request institutional pricing.