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J Med Microbiol 55 (2006), 947-952; DOI: 10.1099/jmm.0.46348-0
© 2006 Society for General Microbiology
ISSN 1473-5644

Chlamydia pneumoniae infection of microglial cells in vitro: a model of microbial infection for neurological disease

Hideaki Ikejima1,2, Herman Friedman1 and Yoshimasa Yamamoto1,3

1 Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, Tampa, FL 33612, USA

2 Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki 216-8511, Japan

3 Laboratory of Molecular Microbiology, Department of Basic Laboratory Sciences, Osaka University Graduate School of Medicine, 1-7 Yamadaoka, Suita, Osaka 565-0871, Japan

Correspondence
Yoshimasa Yamamoto
yyamamot{at}sahs.med.osaka-u.ac.jp

Received 28 September 2005
Accepted 9 February 2006

Chlamydia pneumoniae is the aetiological cause of a wide variety of chronic inflammatory diseases and may be associated with neurological disease. Microbiological and immunological aspects of the interaction between C. pneumoniae and the central nervous system (CNS) are not well understood because of the lack of a suitable infection model for neuronal studies. In the present study, an in vitro C. pneumoniae infection model was developed in the established microglial cell line EOC 20. Infection of the cells resulted in obvious induction of proinflammatory cytokines. The infection also selectively induced matrix metalloproteinase-9 (MMP-9) but not MMP-2. Moreover, beta interferon, which is known to modulate CNS disease, inhibited induction of MMP-9 following C. pneumoniae infection. These results support the view that C. pneumoniae infection may be associated with marked alteration of the ability of microglial cells to enhance cytokine production as well as induction of an MMP.

Abbreviations: CNS, central nervous system; IFN-ß, beta interferon; IFU, inclusion-forming units; IL-10, interleukin-10; IL-12, interleukin-12; MMP-9, matrix metalloproteinase-9; MS, multiple sclerosis; TIMP-1, tissue inhibitor of metalloprotease 1; TNF-{alpha}, tumour necrosis factor {alpha}.




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