Abstract
We have previously shown that infection with Chlamydia pneumoniae can significantly exacerbate atherosclerotic lesions in LDLR-/- mice concurrently fed a high cholesterol diet in 6 or 9 months. We now report that a period of 4 month was sufficient for demonstrating the C. pneumoniae atherogenicity. However, heat inactivation of C. pneumoniae organisms completely abolished the ability of C. pneumoniae to exacerbate the atherosclerotic lesions, suggesting that viable organism infection may be required for the C. pneumoniae atherogenicity.
Original language | English (US) |
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Pages (from-to) | 147-152 |
Number of pages | 6 |
Journal | Molecular and Cellular Biochemistry |
Volume | 260 |
Issue number | 1 |
DOIs | |
State | Published - May 2004 |
Keywords
- Atherogenesis
- Chlamydia pneumoniae
- Heat-inactivation
- LDLR-/- murine model
ASJC Scopus subject areas
- Molecular Biology
- Clinical Biochemistry
- Cell Biology