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

¹ Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit MI 48201, USA
² Department of Medicine, Division of Rheumatology, University of Pennsylvania School of Medicine and Medical Research Department Veterans Affairs Medical Center, Philadelphia PA 19104, USA
³ Medical Research, Department of Veterans Affairs Medical Center, Detroit MI 48201, USA

Correspondence to:
Correspondence to:
Dr A P Hudson
Department of Immunology and Microbiology, Wayne State University School of Medicine, Gordon H Scott Hall, 540 East Canfield Avenue, Detroit MI 48201 USA; ahudson{at}med.wayne.edu

Background: 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.

Objective: To investigate whether the pattern of gene expression underlying chlamydial persistence is similar to that underlying mycobacterial persistence.

Methods: 194 genes in M tuberculosis that are transcriptionally up regulated to support in vivo growth and persistence of that organism have previously been identified. Each of those genes was compared with the C trachomatis genome to identify orthologues. Expression of selected chlamydial orthologues so identified was assessed by real time RT-PCR in an in vitro model of chlamydial persistence and synovial tissues from patients who were 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 orthologues fell into similar metabolic and other categories as those in M tuberculosis. Expression of a majority of selected chlamydial orthologues was strongly up regulated in an in vitro model of chlamydial persistence and in synovial tissues of relevant patients, compared with their expression during active infection.

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

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

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