title: Ectopic expression of blood type antigens in inflamed mucosa with higher incidence of FUT2 secretor status in colonic Crohn's disease.
abstract: BACKGROUND
  Host-intestinal microbial interaction plays an important role in the pathogenesis of inflammatory bowel diseases (IBDs). The surface molecules of the intestinal epithelium act as receptors for bacterial adhesion and regulate the intestinal bacteria. Some known receptors are the mucosal blood type antigens, which are regulated by the fucosyltransferase2 (FUT2) gene, and individuals who express these antigens in the gastrointestinal tract are called secretors. Recent research has revealed that the FUT2 gene is associated with Crohn's disease (CD) in western populations.
  
  
  METHODS
  To clarify the contribution of mucosal blood type antigens in IBD, we determined the incidence of five previously reported single-nucleotide polymorphisms of the FUT2 gene in Japanese patients. We also used immunohistochemistry to investigate the antigen expression in mucosal specimens from IBD patients and animal models.
  
  
  RESULTS
  Genetic analysis revealed that all of the patients with colonic CD were secretors, whereas the incidence of secretors was 80, 80, 67, and 80%, respectively, for the control, ileocolonic CD, ileal CD, and ulcerative colitis groups (P = 0.036). Abnormal expression of blood type antigens was observed only in colonic CD. Interleukin-10⁻/⁻ mice, but not dextran sulfate sodium colitis mice, had enhanced colonic expression of blood type antigens, and the expression of these antigens preceded the development of colitis in the interleukin-10⁻/⁻ mice.
  
  
  CONCLUSIONS
  FUT2 secretor status was associated with colonic-type CD. This finding, taken together with the immunohistochemistry data, suggests that the abnormal expression of blood type antigens in the colon may be a unique and essential factor for colonic CD.
authors: Division of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.
authors: Jun
authors: J
authors: Miyoshi
authors: Tomoharu
authors: T
authors: Yajima
authors: Susumu
authors: S
authors: Okamoto
authors: Katsuyoshi
authors: K
authors: Matsuoka
authors: Nagamu
authors: N
authors: Inoue
authors: Tadakazu
authors: T
authors: Hisamatsu
authors: Katsuyoshi
authors: K
authors: Shimamura
authors: Atsushi
authors: A
authors: Nakazawa
authors: Takanori
authors: T
authors: Kanai
authors: Haruhiko
authors: H
authors: Ogata
authors: Yasushi
authors: Y
authors: Iwao
authors: Makio
authors: M
authors: Mukai
authors: Toshifumi
authors: T
authors: Hibi
mesh_terms: D000328:Adult; D000818:Animals; D044466:Asian People / Q000235:genetics; D001789:Blood Group Antigens / Q000235:genetics*; D016022:Case-Control Studies; D003093:Colitis, Ulcerative / Q000235:genetics; D003106:Colon / Q000503:physiopathology; D003424:Crohn Disease / Q000235:genetics* / Q000276:immunology / Q000503:physiopathology; D004195:Disease Models, Animal; D005260:Female; D005647:Fucosyltransferases / Q000235:genetics*; D020022:Genetic Predisposition to Disease; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics; D007413:Intestinal Mucosa / Q000473:pathology*; D007564:Japan; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D055815:Young Adult; D000097631:Galactoside 2-alpha-L-fucosyltransferase
chemical_list: D001789:Blood Group Antigens; D005647:Fucosyltransferases; D016753:Interleukin-10; D000097631:Galactoside 2-alpha-L-fucosyltransferase