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KMID : 0816120030060010001
Korean Journal of Pediatric Gastroenterolology and Nutrition
2003 Volume.6 No. 1 p.1 ~ p.9
The Genotypes of Helicobacter pylori, Gastric Epithelial Cell Proliferation and Apoptosis in Children
Jung Ji-Ah

Lee Mi-Ae
Seo Jung-Wan
Abstract
PURPOSE: To investigate the relation of the gastric epithelial cell proliferation, apoptosis and genotypes of H. pylori in children.

METHODS: Histologic grading by updated Sydney system, PCNA immunostaining, TUNEL method and the genotypes (cagA, picB and iceA) by PCR were performed in H. pylori positive (N=20) and negative (N=20) gastric biopsy specimens.

RESULTS: PCNA index was significantly different between H. pylori positive children (77.4+/-13.12) and H. pylori negative children (52.3+/-12.20)(p=0.000). There were positive correlations between PCNA index and H. pylori density (r=0.624, p=0.000), polymorphonuclear neutrophil activity (r=0.460, p=0.005) and chronic inflammation (r=0.433, p=0.009). Apoptosis index of H. pylori positive children (0.70+/-0.411) was significantly higher than of H. pylori negative children (0.14+/-0.201) (p=0.000). Positive correlations between apoptosis index and H. pylori density (r=0.691, p=0.000), polymorphonuclear neutrophil activity (r=0.585, p=0.000) and chronic inflammation (r=0.535, p=0.001) were noted. As PCNA index increased, apoptosis index significantly increased (r=0.527, p=0.001). The positive rates of genotypes were cagA 90%, picB 75%, iceA1 60% and iceA2 15%, respectively. There were no significant correlations between the status of the genotypes and PCNA index, apoptosis index, the endoscopic findings and the histologic findings.

CONCLUSION: PCNA index and apoptosis index in H. pylori positive children were higher than in H. pylori negative children but were not related to H. pylori genotypes. This study suggested that correlatively increased gastric epithelial cell proliferation and apoptosis are important to pathogenesis of H. pylori infection in children.
KEYWORD
Helicobacter pylori, Gastric epithelial cell, Proliferation, Apoptosis, cagA, picB, iceA
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