Elevated serum anti-flagellin antibodies implicate subclinical bowel inflammation in ankylosing spondylitis: an observat
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RESEARCH ARTICLE
Open Access
Elevated serum anti-flagellin antibodies implicate subclinical bowel inflammation in ankylosing spondylitis: an observational study Dinny Wallis1, Arundip Asaduzzaman1, Michael Weisman2, Nigil Haroon1, Ammepa Anton1, Dermot McGovern2, Stephan Targan2 and Robert Inman1*
Abstract Introduction: Ankylosing spondylitis (AS) and inflammatory bowel disease (IBD) share genetic and clinical features. IBD is associated with the presence of antibodies to a variety of commensal microorganisms including anti-Saccharomyces cerevesiae antibodies (ASCA), antineutrophil cytoplasmic antibodies (ANCA), anti-I2 (associated with anti-Pseudomonas activity), anti-Eschericia coli outer membrane porin C (anti-OmpC) and anti-flagellin antibodies (anti-CBir1). Subclinical intestinal inflammation may be present in up to 65% of patients with AS. This study evaluated the presence of antimicrobial antibodies in patients with AS alone, patients with AS and concomitant IBD (AS-IBD) and a control group of patients with mechanical back pain (MBP). Methods: Sera were tested by ELISA for ASCA IgG and IgA, anti-OmpC, anti-CBir1 and ANCA in 76 patients with AS alone, 77 patients with AS-IBD and 48 patients with MBP. Antibody positivity rates, median quantitative antibody levels and the proportion of patients with antibody levels in the 4th quartile of a normal distribution were compared between the three groups of patients. Results: Patients with AS alone demonstrated higher anti-CBir1 antibody positivity rates and median antibody levels than MBP patients. Anti-CBir1 positivity in AS was associated with elevation of acute phase reactants. AS-IBD patients demonstrated elevated responses when compared to AS alone for ASCA, anti-OmpC and anti-CBir1. Quartile analysis confirmed the findings. Conclusions: These data suggest that adaptive immune responses to microbial antigens occur in AS patients without clinical IBD and support the theory of mucosal dysregulation as a mechanism underlying the pathophysiology of AS.
Introduction Ankylosing spondylitis (AS) is a chronic inflammatory arthritis characterized by inflammation of the joints of the spine, tendons and entheses. An association between AS and inflammatory bowel disease (IBD) has been recognized for many years. Evidence of intestinal inflammation, which may be subclinical, is present in up to 65% of patients with spondyloarthritis (SpA) [1]. In axial spondyloarthritis, subclinical gut inflammation has been shown to be independently associated with male sex, high disease activity, restricted spinal mobility and shorter symptom duration [2]. There is evidence to support a common genetic * Correspondence: [email protected] 1 Toronto Western Hospital, University of Toronto, 399 Bathurst St, Toronto M5T 2S8, ON, Canada Full list of author information is available at the end of the article
component for AS and IBD, as evidenced by a study of families of AS probands in Iceland [3]. Further work has shown that a single nucleotide polymorphism (SNP) in the IL-23R) gene on chr
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