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Heat-inactivated C. pneumoniae organisms are not atherogenic

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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.

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Authors and Affiliations

  1. Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX, 78229, USA

    Jyotika Sharma & Guangming Zhong

  2. Shanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, 200032, China

    Yuhong Niu & Jianbo Ge

  3. St. Boniface General Hospital Research Centre and the Department of Physiology, University of Manitoba, Winnipeg, Manitoba, R2H 2A6, Canada

    Grant N. Pierce

Authors
  1. Jyotika Sharma
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  2. Yuhong Niu
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  4. Grant N. Pierce
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  5. Guangming Zhong
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Sharma, J., Niu, Y., Ge, J. et al. Heat-inactivated C. pneumoniae organisms are not atherogenic. Mol Cell Biochem 260, 147–152 (2004). https://doi.org/10.1023/B:MCBI.0000026066.64125.71

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  • DOI: https://doi.org/10.1023/B:MCBI.0000026066.64125.71

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