Membrane-bound mucins and mucin terminal glycans expression in idiopathic or helicobacter pylori, NSAID associated peptic ulcers

Yaron Niv*, 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

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

3 Scopus citations

Abstract

Background The ratio of Helicobacter pylori/NSAIDnegative 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. Aims 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 a2-6 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.

Original languageEnglish
Pages (from-to)2535-2544
Number of pages10
JournalDigestive Diseases and Sciences
Volume57
Issue number10
DOIs
StatePublished - Oct 2012

Funding

FundersFunder number
National Institute of Neurological Disorders and StrokeP30NS047101
National Institute of Neurological Disorders and Stroke

    Keywords

    • ECA
    • Helicobacter pylori
    • Idiopathic ulcer
    • MUC1
    • MUC17
    • MUC4
    • Mucin
    • SNA

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