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Mechanisms of Disease: infection and spondyloarthritis

Nature Clinical Practice Rheumatology volume 2, pages 163–169 (2006)Cite this article

Abstract

There is compelling evidence that some infections can initiate a chronic nonseptic arthritis. This has proved to be an important area of investigation into gene–environment interactions, particularly since HLA-B27 confers increased susceptibility to reactive arthritis. This research has investigated the microbiology of these events, and the strategies used by pathogens to induce chronic joint inflammation. Insights into the HLA-orchestrated immune response in this context have also shed light on the impact of HLA-B27 on immunity, which might provide insights into the mechanism of other HLA-B27-associated diseases. Despite the genetic link to reactive arthritis, there is no proven relationship between ankylosing spondylitis and an inciting infection. In general, most trials have found antibiotics to be ineffective in modifying the course of spondyloarthritis.

Key Points

  • Infection is the initiating event in reactive arthritis, which can become chronic arthritis

  • The basis of this event is not understood but HLA-B27 might modulate immune responses to the pathogen

  • The role of infection in other HLA-B27-associated diseases, such as ankylosing spondylitis, has not been proven

  • Antibiotics have generally not been shown to be effective in spondyloarthritis trials

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Figure 1: Spondyoarthritis subsets.
Figure 2: Factors involved in the pathogenesis of the various spondyoarthritis subsets.

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Authors and Affiliations

  1. Director of the Arthritis Center of Excellence, University Health Network, and is a Professor of Medicine and Immunology at the University of Toronto, Toronto, ON, Canada

    Robert D Inman

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  1. Robert D Inman
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Correspondence to Robert D Inman.

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Inman, R. Mechanisms of Disease: infection and spondyloarthritis. Nat Rev Rheumatol 2, 163–169 (2006). https://doi.org/10.1038/ncprheum0118

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  • DOI: https://doi.org/10.1038/ncprheum0118

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