Digestive Diseases and Sciences

, Volume 57, Issue 10, pp 2535–2544 | Cite as

RETRACTED ARTICLE: Membrane-Bound Mucins and Mucin Terminal Glycans Expression in Idiopathic or Helicobacter pylori, NSAID Associated Peptic Ulcers

  • Yaron NivEmail author
  • Doron Boltin
  • Marisa Halpern
  • Miriam Cohen
  • Zohar Levi
  • Alex Vilkin
  • Sara Morgenstern
  • Vahig Manugian
  • Erica St. Lawrence
  • Pascal Gagneux
  • Surinder K. Batra
  • Samuel B. Ho
Original Article



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.


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.


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.


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.


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.


Idiopathic ulcer Mucin MUC1 MUC4 MUC17 SNA ECA Helicobacter pylori 



The work was supported by National Institute of Neurological Disorders and Stroke (grant P30 NS047101; Neurosciences Microscopy Shared Facility, UCSD) and grant *** CSD018 from the G. Harold and Leila Y. Mathers Charitable Foundation (P. Gagneux). Sukhwinder Kaur, Srustidhar Das, and Poonam Sharma performed the MUC4 staining.

Conflict of interest

None declared.


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Copyright information

© Springer Science+Business Media, LLC 2012

Authors and Affiliations

  • Yaron Niv
    • 1
    Email author
  • Doron Boltin
    • 1
  • Marisa Halpern
    • 2
  • Miriam Cohen
    • 3
  • Zohar Levi
    • 1
  • Alex Vilkin
    • 1
  • Sara Morgenstern
    • 4
  • Vahig Manugian
    • 5
    • 6
  • Erica St. Lawrence
    • 5
    • 6
  • Pascal Gagneux
    • 3
  • Surinder K. Batra
    • 7
  • Samuel B. Ho
    • 5
    • 6
  1. 1.Department of Gastroenterology, Rabin Medical CenterTel Aviv UniversityPetach TikvaIsrael
  2. 2.Department of Pathology, Rabin Medical CenterHasharon HospitalPetach TikvaIsrael
  3. 3.Department of Cellular and Molecular Medicine, Glycobiology Research and Training CenterUniversity of California at San DiegoSan DiegoUSA
  4. 4.Department of Pathology, Rabin Medical CenterBeilinson HospitalPetach TikvaIsrael
  5. 5.Department of MedicineUniversity of CaliforniaSan DiegoUSA
  6. 6.VA San Diego Healthcare SystemSan DiegoUSA
  7. 7.Department of Biochemistry and Molecular BiologyUniversity of NebraskaOmahaUSA

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