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, Sukhwinder Kaur, Poonam K Sharma, Surinder K. Batra, Samuel B. Ho

Research output: Contribution to journalArticle

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Abstract

AIM: To determine the expression of membrane-bound mucins and glycan side chain sialic acids in Helicobacter pylori (H. pylori )-associated, non-steroidal inflammatory drug (NSAID)-associated and idiopathic-gastric ulcers. METHODS: We studied a cohort of randomly selected 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 MUC1, MUC4, MUC17, and staining for Erythrina cristagalli agglutinin and Sambucus nigra agglutinin (SNA) lectins was performed on sections from the ulcer margins. RESULTS: Staining intensity of MUC17 was higher in H. pylori ulcers (group 1) than in idiopathic ulcers (group 4), 11.05 ± 3.67 vs 6.93 ± 4.00 for foveola cells, and 10.29 ± 4.67 vs 8.00 ± 3.48 for gland cells, respectively (P <0.0001). In contrast, MUC1 expression was higher in group 4 compared group 1, 9.89 ± 4.17 vs 2.93 ± 5.13 in foveola cells and 7.63 ± 4.60 vs 2.57± 4.50 for glands, respectively (P <0.0001). SNA lectin staining was increased in group 4, in parallel to elevated MUC1 expression, indicating more abundant α2-6 sialylation in that group. CONCLUSION: Cytoplasmic MUC17 staining was significantly decreased in the cases with idiopathic ulcer. The opposite was observed for both MUC1 and SNA lectin. This observation may reflect important pathogenic mechanisms, since different mucins with altered sialylation patterns may differ in their protection efficiency against acid and pepsin.

Original languageEnglish
Pages (from-to)14913-14920
Number of pages8
JournalWorld Journal of Gastroenterology
Volume20
Issue number40
DOIs
StatePublished - Oct 28 2014

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Agglutinins
Mucins
Peptic Ulcer
Helicobacter pylori
Ulcer
Polysaccharides
Stomach Ulcer
Staining and Labeling
Membranes
Pharmaceutical Preparations
Erythrina
Sialic Acids
Pepsin A
Immunohistochemistry
Acids
Sambucus nigra lectins

All Science Journal Classification (ASJC) codes

  • Gastroenterology
  • Medicine(all)

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Membrane-bound mucins and mucin terminal glycans expression in idiopathic or Helicobacter pylori, NSAID associated peptic ulcers. / Niv, Yaron; Boltin, Doron; Halpern, Marisa; Cohen, Miriam; Levi, Zohar; Vilkin, Alex; Morgenstern, Sara; Manugian, Vahig; St Lawrence, Erica; Gagneux, Pascal; Kaur, Sukhwinder; Sharma, Poonam K; Batra, Surinder K.; Ho, Samuel B.

In: World Journal of Gastroenterology, Vol. 20, No. 40, 28.10.2014, p. 14913-14920.

Research output: Contribution to journalArticle

Niv, Y, Boltin, D, Halpern, M, Cohen, M, Levi, Z, Vilkin, A, Morgenstern, S, Manugian, V, St Lawrence, E, Gagneux, P, Kaur, S, Sharma, PK, Batra, SK & Ho, SB 2014, 'Membrane-bound mucins and mucin terminal glycans expression in idiopathic or Helicobacter pylori, NSAID associated peptic ulcers', World Journal of Gastroenterology, vol. 20, no. 40, pp. 14913-14920. https://doi.org/10.3748/wjg.v20.i40.14913
Niv, Yaron ; Boltin, Doron ; Halpern, Marisa ; Cohen, Miriam ; Levi, Zohar ; Vilkin, Alex ; Morgenstern, Sara ; Manugian, Vahig ; St Lawrence, Erica ; Gagneux, Pascal ; Kaur, Sukhwinder ; Sharma, Poonam K ; Batra, Surinder K. ; Ho, Samuel B. / Membrane-bound mucins and mucin terminal glycans expression in idiopathic or Helicobacter pylori, NSAID associated peptic ulcers. In: World Journal of Gastroenterology. 2014 ; Vol. 20, No. 40. pp. 14913-14920.
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abstract = "AIM: To determine the expression of membrane-bound mucins and glycan side chain sialic acids in Helicobacter pylori (H. pylori )-associated, non-steroidal inflammatory drug (NSAID)-associated and idiopathic-gastric ulcers. METHODS: We studied a cohort of randomly selected 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 MUC1, MUC4, MUC17, and staining for Erythrina cristagalli agglutinin and Sambucus nigra agglutinin (SNA) lectins was performed on sections from the ulcer margins. RESULTS: Staining intensity of MUC17 was higher in H. pylori ulcers (group 1) than in idiopathic ulcers (group 4), 11.05 ± 3.67 vs 6.93 ± 4.00 for foveola cells, and 10.29 ± 4.67 vs 8.00 ± 3.48 for gland cells, respectively (P <0.0001). In contrast, MUC1 expression was higher in group 4 compared group 1, 9.89 ± 4.17 vs 2.93 ± 5.13 in foveola cells and 7.63 ± 4.60 vs 2.57± 4.50 for glands, respectively (P <0.0001). SNA lectin staining was increased in group 4, in parallel to elevated MUC1 expression, indicating more abundant α2-6 sialylation in that group. CONCLUSION: Cytoplasmic MUC17 staining was significantly decreased in the cases with idiopathic ulcer. The opposite was observed for both MUC1 and SNA lectin. This observation may reflect important pathogenic mechanisms, since different mucins with altered sialylation patterns may differ in their protection efficiency against acid and pepsin.",
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AU - Niv, Yaron

AU - Boltin, Doron

AU - Halpern, Marisa

AU - Cohen, Miriam

AU - Levi, Zohar

AU - Vilkin, Alex

AU - Morgenstern, Sara

AU - Manugian, Vahig

AU - St Lawrence, Erica

AU - Gagneux, Pascal

AU - Kaur, Sukhwinder

AU - Sharma, Poonam K

AU - Batra, Surinder K.

AU - Ho, Samuel B.

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N2 - AIM: To determine the expression of membrane-bound mucins and glycan side chain sialic acids in Helicobacter pylori (H. pylori )-associated, non-steroidal inflammatory drug (NSAID)-associated and idiopathic-gastric ulcers. METHODS: We studied a cohort of randomly selected 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 MUC1, MUC4, MUC17, and staining for Erythrina cristagalli agglutinin and Sambucus nigra agglutinin (SNA) lectins was performed on sections from the ulcer margins. RESULTS: Staining intensity of MUC17 was higher in H. pylori ulcers (group 1) than in idiopathic ulcers (group 4), 11.05 ± 3.67 vs 6.93 ± 4.00 for foveola cells, and 10.29 ± 4.67 vs 8.00 ± 3.48 for gland cells, respectively (P <0.0001). In contrast, MUC1 expression was higher in group 4 compared group 1, 9.89 ± 4.17 vs 2.93 ± 5.13 in foveola cells and 7.63 ± 4.60 vs 2.57± 4.50 for glands, respectively (P <0.0001). SNA lectin staining was increased in group 4, in parallel to elevated MUC1 expression, indicating more abundant α2-6 sialylation in that group. CONCLUSION: Cytoplasmic MUC17 staining was significantly decreased in the cases with idiopathic ulcer. The opposite was observed for both MUC1 and SNA lectin. This observation may reflect important pathogenic mechanisms, since different mucins with altered sialylation patterns may differ in their protection efficiency against acid and pepsin.

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