title: Membrane-bound mucins and mucin terminal glycans expression in idiopathic or Helicobacter pylori, NSAID associated peptic ulcers.
abstract: BACKGROUND
  The ratio of Helicobacter pylori/NSAID-negative gastric ulcers is increasing. Idiopathic gastric ulcers have unique clinical and endoscopic features, and are associated with more bleeding complications and a higher mortality. Alterations in gastric mucin expression and sialylation pattern may be important in ulcer pathogenesis.
  
  
  OBJECTIVE
  The purpose of this study was to determine the expression pattern of membrane-bound mucins and side chain sugars in H. pylori associated-, NSAID-, and idiopathic-gastric ulcers.
  
  
  METHODS
  We randomly selected 92 patients with H. pylori (group 1, n = 30), NSAID (group 2, n = 18), combined H. pylori and NSAID associated gastric ulcers (group 3, n = 24), and patients with idiopathic gastric ulcers (group 4, n = 20). Immunohistochemistry for T-cell CD4/CD8, MUC1, MUC4, MUC17, and ECA and SNA lectins staining was performed on sections from the ulcer margins. Inflammation score was assessed according to the Sydney system.
  
  
  RESULTS
  Bleeding and mortality rates were significantly higher in group 4. CD4 positive T cell count was higher in H. pylori positive patients (P = 0.009). Staining intensity of MUC17 was higher in group 1 than in group 4, foveola and glands alike, with 11.50 ± 3.47 versus 6.80 ± 4.02, and 9.61 ± 4.26 versus 7.59 ± 3.26, respectively (P < 0.0001). This was a mirror image with MUC1. SNA lectin staining was increased in group 4, in parallel to MUC1 expression, indicating more abundant α2-6 sialylation in that group.
  
  
  CONCLUSIONS
  Cytoplasmic MUC17 staining was significantly decreased in the cases with idiopathic ulcer. The opposite was demonstrated for MUC1. This observation might be important, since different mucins with altered sialylation patterns likely differ in their protection efficiency against acid and pepsin.
authors.affiliation: Department of Gastroenterology, Rabin Medical Center, Tel Aviv University, 39 Jabotinski Street, 49100 Petach Tikva, Israel. nivyaron80@gmail.com
authors.forename: Yaron
authors.initials: Y
authors.lastname: Niv
authors.forename: Doron
authors.initials: D
authors.lastname: Boltin
authors.forename: Marisa
authors.initials: M
authors.lastname: Halpern
authors.forename: Miriam
authors.initials: M
authors.lastname: Cohen
authors.forename: Zohar
authors.initials: Z
authors.lastname: Levi
authors.forename: Alex
authors.initials: A
authors.lastname: Vilkin
authors.forename: Sara
authors.initials: S
authors.lastname: Morgenstern
authors.forename: Vahig
authors.initials: V
authors.lastname: Manugian
authors.forename: Erica
authors.initials: E
authors.lastname: St Lawrence
authors.forename: Pascal
authors.initials: P
authors.lastname: Gagneux
authors.forename: Surinder K
authors.initials: SK
authors.lastname: Batra
authors.forename: Samuel B
authors.initials: SB
authors.lastname: Ho
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D016516:CD4-CD8 Ratio; D005260:Female; D005752:Gastric Mucins / Q000737:chemistry / Q000378:metabolism*; D006471:Gastrointestinal Hemorrhage / Q000209:etiology; D005786:Gene Expression Regulation / Q000502:physiology; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D037102:Lectins / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010437:Peptic Ulcer / Q000209:etiology* / Q000378:metabolism*; D011134:Polysaccharides / Q000737:chemistry / Q000378:metabolism; D055815:Young Adult
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D005752:Gastric Mucins; D037102:Lectins; D011134:Polysaccharides