This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rödel, J.
Right arrow Articles by Straube, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rödel, J.
Right arrow Articles by Straube, E.

 Previous Article  |  Next Article 

Infection and Immunity, August 2004, p. 4900-4904, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4900-4904.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Chlamydia pneumoniae Decreases Smooth Muscle Cell Proliferation through Induction of Prostaglandin E2 Synthesis

Jürgen Rödel,1* Dirk Prochnau,2 Katrin Prager,1 Jürgen Baumert,1 Karl-Hermann Schmidt,1 and Eberhard Straube1

Institute of Medical Microbiology,1 Clinic of Internal Medicine, Department of Cardiology, Friedrich Schiller University of Jena, D-07740 Jena, Germany2

Received 23 January 2004/ Returned for modification 25 February 2004/ Accepted 27 April 2004

Chlamydia pneumoniae may modulate the proliferation of smooth muscle cells (SMC) in atherosclerotic plaques. Conditioned medium from C. pneumoniae-infected SMC decreased the proliferation of uninfected SMC. Treatment of infected cells with the cyclooxygenase-2 inhibitor NS-398 {N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide} suppressed the up-regulation of prostaglandin E2 (PGE2) and abolished the antimitogenic effect of conditioned medium, suggesting that C. pneumoniae can decrease SMC proliferation via stimulation of PGE2 synthesis.

* Corresponding author. Mailing address: Institute of Medical Microbiology, Friedrich Schiller University of Jena, Semmelweisstr. 4, D-07740 Jena, Germany. Phone: 49-3641-933105. Fax: 49-3641-933474. E-mail: juergen.roedel{at}med.uni-jena.de.

Editor: J. N. Weiser

Infection and Immunity, August 2004, p. 4900-4904, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4900-4904.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Bobryshev, Y. V., Lord, R. S. A., Tran, D. (2006). Chlamydia pneumoniae in foci of "early" calcification of the tunica media in arteriosclerotic arteries: an incidental presence?. Am. J. Physiol. Heart Circ. Physiol. 290: H1510-H1519 [Abstract] [Full Text]  
  • Hauer, A.D., de Vos, P., Peterse, N., ten Cate, H., van Berkel, Th.J.C., Stassen, F.R.M., Kuiper, J. (2006). Delivery of Chlamydia pneumoniae to the vessel wall aggravates atherosclerosis in LDLr-/- mice. Cardiovasc Res 69: 280-288 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»