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.M...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(group4),11.05±3.67 vs 6.93±4.00 for foveola cells,and10.29±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 MUC1expression,indicating more abundantα2-6 sialylation in that group.CONCLUSION:Cytoplasmic MUC17 staining was sig-nificantly 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.展开更多
基金Supported by National Institute of Neurological Disorders and Stroke No.P30 NS047101Neurosciences Microscopy Shared Facility,UCSD from the G Harold and Leila Y Mathers Charitable Foundation No.CSD018NIH center grant No.DK080506
文摘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(group4),11.05±3.67 vs 6.93±4.00 for foveola cells,and10.29±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 MUC1expression,indicating more abundantα2-6 sialylation in that group.CONCLUSION:Cytoplasmic MUC17 staining was sig-nificantly 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.
