Mechanisms of disease: infection and spondyloarthritis.
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.
Inman
Robert D
RD
Arthritis Center of Excellence, University Health Network, University of Toronto, Toronto, ON, Canada. robert.inman@uhn.on.ca
D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D016918:Arthritis, Reactive / Q000382:microbiology; D001424:Bacterial Infections / Q000150:complications* / Q000188:drug therapy / Q000276:immunology; D020022:Genetic Predisposition to Disease; D015796:HLA-B27 Antigen / Q000235:genetics / Q000276:immunology; D006801:Humans; D025241:Spondylarthritis / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology
D000900:Anti-Bacterial Agents; D015796:HLA-B27 Antigen