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09:52
A Mouse Model for Pathogen-induced Chronic Inflammation at Local and Systemic Sites
Published on: August 8, 2014
Anti-P. gingivalis response correlates with atherosclerosis
1Oral Biology and Pathology, School of Dentistry, University of Queensland, Brisbane 4072, Australia. p.ford@uq.edu.au
Journal of Dental Research
|December 26, 2006
Summary
Porphyromonas gingivalis infection, but not Chlamydia pneumoniae, exacerbated atherosclerosis in mice. Molecular mimicry involving heat-shock protein GroEL and host HSP60 may drive this process.
Area of Science:
- Cardiovascular Research
- Infectious Diseases
- Immunology
Background:
- Atherosclerosis is linked to pathogens like Porphyromonas gingivalis and Chlamydia pneumoniae.
- Seropositivity to these pathogens is common in individuals with atherosclerosis.
Purpose of the Study:
- To investigate the atherogenic impact of P. gingivalis and C. pneumoniae.
- To explore the role of molecular mimicry between bacterial GroEL and host HSP60.
Main Methods:
- Atherogenesis was studied in apolipoprotein-E-deficient mice.
- Mice were immunized with P. gingivalis, C. pneumoniae, or both.
- Aortic lesion area and serum antibody levels were measured.
Main Results:
- P. gingivalis infection, not C. pneumoniae, increased atherosclerosis.
- Host HSP60 was found in atherosclerotic lesions.
- Anti-GroEL antibody levels correlated with lesion development in P. gingivalis-immunized mice.
Conclusions:
- P. gingivalis contributes to atherogenesis, potentially via molecular mimicry.
- Molecular mimicry between GroEL and host HSP60 is implicated in atherosclerosis.
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