Objective: The importance of the presence of bacterial antigen or even living bacteria for the pathogenesis of reactive arthritis has been discussed increasingly ever since bacterial antigen was found in inflamed joints. Bacteria may persist in the body and drive the local immune response, maintaining arthritis. Cytokines, in particular tumor necrosis factor-alpha (TNF-alpha) are essential for bacterial elimination. In reactive arthritis, the course of the disease is influenced by several cytokines, including TNF-alpha. TNF-alpha expression can be mediated by transcription factor nuclear factor-kappa B (NF-kappaB). Moreover, TNF-alpha is also one of the strongest activators of NF-kappaB.
Methods: In vitro expression of TNF-alpha and activation of NF-kappaB in synovial fibroblasts after infection with Yersinia enterocolitica or Salmonella enteritidis was analysed by electrophoretic mobility shift assay, Western blot assay and real-time PCR.
Results: We found that infection of synovial fibroblasts with yersinia and salmonellae lead to the transient expression of TNF-alpha mRNA and induction of NF-kappaB.
Conclusion: Induction of TNF-alpha in synovial fibroblasts after infection with yersiniae or salmonellae might be insufficient to eliminate bacteria, and this could allow the intracellular persistence of these bacteria. Our results therefore support the hypothesis that a permissive cytokine pattern might contribute to the pathogenesis of reactive arthritis.