Inflammation in HLA-B27-associated Diseases

Abstract

The pathogenetic mechanisms in the development of spondyloarthropathies are multifactorial. These include the possible role of infective micro-organisms which can by direct invasion lead to persistence of microbial antigens and thus trigger arthritis or by cross-reactions with the host tissue lead to inflammatory symptoms or by cross-reactions with HLA-B27 trigger cytotoxic T-cell response. After the primary event, exaggerated inflammatory response can lead to amplification of inflammation. The components in the amplification of inflammation include hyperreactive neutrophils and serum factors such as enhanced production of activation products of complement in subjects with HLA-B27. The enhanced neutrophil function seems to persist in patients with previous severe inflammatory symptoms during acute reactive arthritis or in those with late inflammatory complications. The enhancement is probably caused by priming effect by lipopolysaccharide, which seems to persist for a long period in patients with acute reactive arthritis. Enhanced production of monokines can contribute to the enhanced inflammation in patients with spondyloarthropathies. The primed phagocytes can respond vigorously when rechallenged with antigenic load during a new infection, thus leading in some patients to recurrent or chronic inflammatory symptoms. Antimicrobial therapy or sulphasalazine by modifying antigen elimination or absorption can diminish inflammatory response during acute arthritis and in chronic spondyloarthropathies. Long-term follow-up studies are needed to find out whether prolonged therapies with these agents affect the prognosis of spondyloarthropathies.