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Microbiology 148 (2002), 3955-3959
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Microbiology (2002), 148, 3955-3959.
© 2002 Society for General Microbiology

Research Paper

Infection of myocytes with chlamydiae

Guqi Wang1, Frank Burczynski1, Brian Hasinoff1 and Guangming Zhong2

Faculty of Pharmacy, University of Manitoba, Winnipeg, Manitoba R3T 2N2, Canada1
Department of Microbiology and Immunology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA2

Author for correspondence: Guangming Zhong. Tel: +1 210 567 1169. Fax: +1 210 567 0293. e-mail: Zhongg{at}UTHSCSA.edu

Chlamydial infection has been associated with myocarditis in animals and humans. However, the mechanism resulting in myocarditis following infection is not known. Here, evidence is presented that both Chlamydia trachomatis and Chlamydia pneumoniae can infect and replicate in myocytes isolated from neonate rats. The infected myocytes contained chlamydial inclusions, indicative of chlamydial growth, and infectious particles were recovered from the infected myocytes. It was also found that chlamydial infection at a late stage induced significant damage to the infected myocytes, as evidenced by an increased lactate dehydrogenase release, reactive oxygen species production and a reduced ATP level. However, no nuclear apoptosis was detected in the infected myocytes. Collectively, these observations have demonstrated that Chlamydia spp. are able to both infect and damage myocytes, suggesting a potential role of chlamydial infection in myocarditis.

Keywords: myocarditis, myocytes, chlamydial infection, apoptosis

Abbreviations: i.f.u., inclusion-forming unit(s); LDH, lactate dehydrogenase




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