The change of gastric antral mucin expression after Helicobacter pylori eradication.
- Author:
Myung Sin MA
1
;
Jin Su HWANG
;
Sung Il NA
;
Kil Hong LEE
;
Jeong Ki CHOI
;
Seung Ok LEE
;
Myoung Jae KANG
;
Dae Ghon KIM
;
Deuk Soo AHN
;
Soo Teik LEE
Author Information
1. Department of Internal Medicine, Chonbuk National University Medical School, Chonju, Korea. Soo@moak.chunbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Mucin;
Helicobacter pylori;
MUC5AC;
Eradication
- MeSH:
Biopsy;
Breath Tests;
Colon;
Epithelial Cells;
Epithelium;
Gastric Mucins;
Helicobacter pylori*;
Helicobacter*;
Humans;
Immunohistochemistry;
Mucins*;
Mucus;
Urea
- From:Korean Journal of Medicine
2003;64(1):21-27
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Helicobacter pylori colonizes the gastric surface epithelium and the mucus gel layer. It has been known that H. pylori infection decreased the gastric mucin expression. The aim of this study was to determine the effect of H. pylori eradication on mucin expression (MUC5AC, MUC6 and MUC1) in the gastric epithelium. METHODS: This study included 20 patients positive for H. pylori whom successful eradication was performed between March 1998 and December 1999. H. pylori status was determined by histology, rapid urase test and urea breath test. Gastric antral biopsy specimens were examined by immunohistochemistry for mucin (MUC5AC, MUC6 and MUC1) expression. The distribution of epithelial cells expressing MUC5AC was calculated at two sites (surface mucous cells, pyloric glands). Two scores system (weak-strong) was used to assess staining intensity. RESULTS: There was a gradient of MUC5AC expression, higher to lower from the surface to the glands. Increased MUC5AC expression in the surface mucous cell (p=0.013) and in the glands (p=0.008) was found after H. pylori eradication. MUC6 and MUC1 distribution was not changed after H. pylori eradication. CONCLUSION: MUC5AC expression was increased after H. pylori eradication. These results suggest that MUC5AC may relate in the pathogenesis of H. pylori.
