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Rheumatology Advance Access published online on October 13, 2006
Rheumatology, doi:10.1093/rheumatology/kel348
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© The Author 2006. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received July 2, 2006
Accepted September 8, 2006

Original Papers

Role of TNFRp55 in Yersinia enterocolitica O:3-induced arthritis: triggering bacterial antigens and articular immune response

M. S. Di Genaro 1 *, D. E. Cargnelutti 1, J. R. Eliçabe 1, M. G. Lacoste 1, S. Valdez 2, N. Gómez 1, and A. M. S. de Guzmán 1

1 Laboratory of Microbiology and Immunology, Faculty of Chemistry, Biochemistry and Pharmacy, National University of San Luis, 5700, San Luis, Argentina
2 LARLAC (CONICET) Faculty of Medicine, National University of Mendoza, 5500, Mendoza, Argentina

* To whom correspondence should be addressed.
M. S. Di Genaro, E-mail: sdigena{at}unsl.edu.ar


  Abstract

Objectives. The pathogenesis of reactive arthritis (ReA), an aseptic synovitis that follows an extra-articular infection, is incompletely known. We studied the impact of tumour necrosis factor receptor (TNFR) p55 deficiency on the progression to ReA after oral Yersinia enterocolitica O:3 infection, the Yersinia antigens triggering articular inflammation and a possible articular TNFRp55-mediated mechanism that protects against ReA.

Methods. Wild-type C57BL/6 and TNFRp55-/- mice were orogastrically infected with Y. enterocolitica O:3 and monitored for survival and arthritis development. The bacterial load was determined in mesenteric lymph nodes (MLNs), the spleen and joints. Interferon (IFN)-{gamma}, TNF-{alpha} and IL-10 mRNA expression in MLN and joints were analysed by reverse transcription-polymerase chain reaction (RT-PCR). Articular antibodies to Yersinia antigens, TNF-{alpha} protein and nitric oxide (NO) levels were assessed. Acute arthritis was evaluated after joint injection of Yersinia antigens.

Results. The survival rate was 60% in TNFRp55-/- mice. They showed impaired bacterial clearance in MLN, the spleen and joints, and excessive mRNA expression of pro-inflammatory cytokines in MLN. Clinical and histological examinations revealed that TNFRp55-/- mice developed severe arthritis. Moreover, augmented articular outer membrane protein (OMP)-specific antibodies and TNF-{alpha} but impaired NO levels were detected in TNFRp55-/- mice. Synovial inflammatory response was detected by joint OMP injection.

Conclusions. TNFRp55-mediated immune mechanisms prevent ReA development after oral infection with Y. enterocolitica O:3. Yersinia OMPs are the relevant antigens triggering ReA. NO induction through TNFRp55 signalling could have a local antibacterial function to prevent ReA. This study could contribute to ReA-specific therapeutic studies.

Keywords: Yersinia enterocolitica; Reactive arthritis; TNFRp55; Oral infection; Mice; Bacterial antigens; Nitric oxide.
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