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Infection and Immunity, February 2009, p. 867-876, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.00566-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Host Cell Cytokines Induced by Chlamydia pneumoniae Decrease the Expression of Interstitial Collagens and Fibronectin in Fibroblasts{triangledown}

Jürgen Baumert,1 Karl-Hermann Schmidt,1 Annett Eitner,2 Eberhard Straube,1 and Jürgen Rödel1*

Institute of Medical Microbiology,1 Institute of Anatomy II, Friedrich Schiller University of Jena, D-07740 Jena, Germany2

Received 9 May 2008/ Returned for modification 21 August 2008/ Accepted 20 November 2008

Chlamydia pneumoniae infection has been associated with chronic obstructive airway disease (COPD), asthma, and atherosclerosis. Inflammation and airway remodeling in asthma and COPD result in subepithelial fibrosis that is characterized by the deposition of interstitial collagens and fibronectin. The progression of atherosclerosis is also accompanied by an increased production of interstitial collagens in the intima. As shown by reverse transcription-PCR and immunoblotting, infection of human fibroblasts and smooth muscle cells by C. pneumoniae TW-183 downregulated the expression of type I and III collagen and fibronectin, whereas the level of type IV collagen remained unchanged. Conditioned medium from infected fibroblasts as well as epithelial WISH cells also reduced the expression of interstitial collagens and fibronectin in uninfected cells. In experiments using blocking antibodies, beta interferon was found to contribute to the inhibitory effects of conditioned medium collected from infected fibroblasts. In contrast, downregulation of matrix protein expression by conditioned medium from epithelial cells was caused by interleukin-1{alpha}, which was not secreted from fibroblasts following chlamydial infection. C. pneumoniae-mediated inhibition of collagen and fibronectin expression was diminished following transfection of fibroblasts with specific small interfering RNA targeting the transcription factor CCAAT/enhancer-binding protein β. The downregulation of interstitial collagens and fibronectin by the Chlamydia-induced host cell cytokine response may modulate tissue remodeling processes in airway diseases. In atherosclerosis the inhibition of collagen synthesis by C. pneumoniae infection may promote plaque vulnerability, thereby increasing the risk of plaque rupture.

* Corresponding author. Mailing address: Institute of Medical Microbiology, Friedrich Schiller University of Jena, Erlanger Allee 101, D-07740 Jena, Germany. Phone: 49 3641 9393633. Fax: 49 3641 9393502. E-mail: juergen.roedel{at}med.uni-jena.de

{triangledown} Published ahead of print on 1 December 2008.

Editor: J. L. Flynn

Infection and Immunity, February 2009, p. 867-876, Vol. 77, No. 2
0019-9567/09/$08.00+0     doi:10.1128/IAI.00566-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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