title: Elevated serum anti-flagellin antibodies implicate subclinical bowel inflammation in ankylosing spondylitis: an observational study.
abstract: BACKGROUND
  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.
authors.forename: Dinny
authors.initials: D
authors.lastname: Wallis
authors.forename: Arundip
authors.initials: A
authors.lastname: Asaduzzaman
authors.forename: Michael
authors.initials: M
authors.lastname: Weisman
authors.forename: Nigil
authors.initials: N
authors.lastname: Haroon
authors.forename: Ammepa
authors.initials: A
authors.lastname: Anton
authors.forename: Dermot
authors.initials: D
authors.lastname: McGovern
authors.forename: Stephan
authors.initials: S
authors.lastname: Targan
authors.forename: Robert
authors.initials: R
authors.lastname: Inman
mesh_terms: D000328:Adult; D000704:Analysis of Variance; D000906:Antibodies / Q000097:blood / Q000276:immunology*; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000097:blood / Q000276:immunology; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology; D000908:Antibodies, Fungal / Q000097:blood / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005408:Flagellin / Q000276:immunology*; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D015212:Inflammatory Bowel Diseases / Q000097:blood / Q000276:immunology* / Q000382:microbiology; D008297:Male; D008875:Middle Aged; D018272:Porins / Q000276:immunology; D012441:Saccharomyces cerevisiae / Q000276:immunology; D013167:Spondylitis, Ankylosing / Q000097:blood / Q000276:immunology* / Q000382:microbiology
chemical_list: D000906:Antibodies; D019268:Antibodies, Antineutrophil Cytoplasmic; D000907:Antibodies, Bacterial; D000908:Antibodies, Fungal; C502160:CBir1 flagellin; D007074:Immunoglobulin G; C113724:OmpC protein; D018272:Porins; D005408:Flagellin; D007073:Immunoglobulin E