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Updated: Jun 28, 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, Okayama, 700-8558, Japan.
Clinical Reviews in Allergy & Immunology
|November 6, 2008
Summary
Immune responses to heat shock protein 60 (HSP60) from chronic infections may drive atherosclerosis. Helicobacter pylori-HSP60 (Hp-HSP60) specific Th1 responses were linked to disease progression in mice, suggesting molecular mimicry.
Area of Science:
- Immunology
- Cardiovascular Research
- Microbiology
Background:
- Heat shock protein 60 (HSP60) from pathogens is implicated in atherosclerosis.
- High antibodies to HSP60 correlate with coronary artery and cerebrovascular diseases.
- HSP60-specific T lymphocytes may also elevate atherosclerosis risk.
Purpose of the Study:
- To investigate the role of Helicobacter pylori-HSP60 (Hp-HSP60) specific Th1 immune responses in atherosclerosis progression.
- To explore the potential cross-reactivity between Hp-HSP60 and endogenous HSP60 via molecular mimicry.
Main Methods:
- In vitro and in vivo studies using a hyperlipidemic mouse model.
- Analysis of Th1 immune responses elicited by H. pylori infection.
Main Results:
- Hp-HSP60 specific Th1 immune responses were associated with accelerated atherosclerosis in hyperlipidemic mice.
- These Th1 responses might cross-react with endothelial HSP60 due to molecular mimicry.
Conclusions:
- Th1-dominant immune responses to Hp-HSP60 contribute to atherosclerosis progression.
- Molecular mimicry between bacterial and self-HSP60 is a potential mechanism.
- Further research is needed to clarify how endothelial cells present HSP60 epitopes.
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