Synovial Chlamydia trachomatis up-regulates expression of a panel of genes similar to that transcribed by Mycobacterium tuberculosis during persistent infection

Herve C Gerard ¹, Judith A Whittum-Hudson ¹, H Ralph Schumacher ² and Alan P Hudson ^1*

¹ Wayne State University School of Medicine, United States
² University of Pennsylvania Medical School, United States

^* To whom correspondence should be addressed. E-mail: ahudson{at}med.wayne.edu.

Accepted 21 September 2005

Abstract

Objective: Synovial tissues in patients with Chlamydia-associated arthritis are persistently infected by C. trachomatis, an organism for which genetic manipulation is not possible. M. tuberculosis also engages in persistent infection, and because this bacterium is genetically tractable many groups have been able to define transcriptional characteristics of mycobacterial growth and persistence. We investigated whether the pattern of gene expression underlying chlamydial persistence is similar to that underlying mycobacterial persistence.

Methods: A study from another group identified 194 genes in M. tuberculosis that are transcriptionally up-regulated to support in vivo growth and persistence of that organism. We compared each of those genes to the C. trachomatis genome to identify orthologs. Expression of selected chlamydial orthologs so identified was assessed by real time RT-PCR in an in vitro model of chlamydial persistence and synovial tissues from patients PCR-positive for C. trachomatis at that site.

Results: 67 C. trachomatis genes were identified as being orthologous to mycobacterial persistence- related genes, representing 35% of the genes tested. The chlamydial orthologs fall into similar metabolic and other categories as those in M. tuberculosis. Expression of a majority of selected chlamydial orthologs is strongly up-regulated in an in vitro model of chlamydial persistence and in synovial tissues of relevant patients, compared to their expression during active infection.

Conclusions: These observations provide new insight concerning the molecular genetic basis underlying chlamydial persistence, and they indicate that this information can be obtained in some instances by extrapolating observations made in other biologic systems and/or organisms.

Keywords: Chlamydia trachomatis, gene expression, pathogenesis, persistent infection, reactive arthritis

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Rosner, I., Haddad, A., Boulman, N., Feld, J., Avshovich, N., Slobodin, G., Rozenbaum, M. (2007). Pregnancy in rheumatology patients exposed to anti-tumour necrosis factor (TNF)-{alpha} therapy. Rheumatology (Oxford) 46: 1508-1508 [Full Text]  
• Roux, C. H., Brocq, O., Breuil, V., Albert, C., Euller-Ziegler, L. (2007). Pregnancy in rheumatology patients exposed to anti-tumour necrosis factor (TNF)-{alpha} therapy. Rheumatology (Oxford) 46: 695-698 [Abstract] [Full Text]  
• Rihl, M, Kohler, L, Klos, A, Zeidler, H (2006). Persistent infection of Chlamydia in reactive arthritis. Ann Rheum Dis 65: 281-284 [Full Text]