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Updated: Jul 11, 2026
09:52
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Chronic infections and atherosclerosis
Kiyoshi Ayada1, Kenji Yokota, Kazuko Kobayashi
1Department of Bacteriology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
Annals of the New York Academy of Sciences
|September 26, 2007
Summary
Chronic Helicobacter pylori infection promotes atherosclerosis in mice through autoimmunity against heat shock protein 60 (HSP60). Targeting HSP60-specific immune responses may reduce atherosclerosis progression.
Area of Science:
- Immunology
- Cardiovascular Science
- Microbiology
Background:
- Chronic infections and immunoinflammatory processes are linked to atherosclerosis development.
- Anti-heat shock protein (HSP) antibodies and HSP60-specific T lymphocytes are associated with increased atherosclerosis risk.
- Helicobacter pylori (H. pylori) infection is implicated in cardiovascular diseases.
Purpose of the Study:
- To investigate the role of H. pylori infection in atherosclerosis progression.
- To explore the involvement of anti-HSP immune responses in H. pylori-induced atherosclerosis.
- To evaluate potential therapeutic strategies targeting HSP60-specific immunity.
Main Methods:
- Utilized apoe+/- ldlr+/- mouse models to study atherosclerosis.
- Induced H. pylori infection and monitored atherosclerosis development.
- Assessed Th1-dominant immune responses specific to H. pylori-derived HSP.
- Investigated molecular mimicry between bacterial and endogenous HSP60.
Main Results:
- H. pylori infection significantly accelerated atherosclerosis in the studied mouse model.
- Hp-anti-HSP specific Th1 immune responses were crucial for atherosclerosis progression.
- Evidence of autoimmunity against endogenous HSP60 on vascular endothelium was observed due to molecular mimicry.
- Reduced atherosclerosis progression was noted with interventions regulating Th1 induction.
Conclusions:
- H. pylori infection can induce atherosclerosis via autoimmune responses against HSP60.
- Molecular mimicry between H. pylori HSP and human HSP60 plays a key role.
- Antibiotic treatment or anti-HSP60 antibody therapy may offer a strategy to mitigate atherosclerosis progression.
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