Heat-inactivated C. pneumoniae organisms are not atherogenic

Jyotika Sharma, Yuhong Niu, Jianbo Ge, Grant N. Pierce, Guangming Zhong

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


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 languageEnglish (US)
Pages (from-to)147-152
Number of pages6
JournalMolecular and Cellular Biochemistry
Issue number1
StatePublished - May 2004


  • Atherogenesis
  • Chlamydia pneumoniae
  • Heat-inactivation
  • LDLR-/- murine model

ASJC Scopus subject areas

  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology


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