DNA Double Strand Breaks in Gastric Epithelium with Helicobacter pylori Infection.
- Author:
Young Jun CHANG
1
;
Sang Won BYUN
;
Hyung Keun KIM
;
Young Seok CHO
;
Sung Soo KIM
;
Jin Il KIM
;
Jae Kwang KIM
;
Eun Sun JUNG
Author Information
- Publication Type:Original Article ; English Abstract ; Research Support, Non-U.S. Gov't
- Keywords: Gastric mucosa; Helicobacter pylori; DNA breaks, double stranded; Gamma-H2AX protein, human; 53BP1 protein, human
- MeSH: Adult; Aged; Aged, 80 and over; Anti-Bacterial Agents/therapeutic use; Cell Line, Tumor; DNA/metabolism; *DNA Breaks, Double-Stranded; Female; Gastric Mucosa/*metabolism; Helicobacter Infections/drug therapy/*metabolism; Helicobacter pylori/*drug effects/pathogenicity; Histones/genetics/metabolism; Humans; Immunohistochemistry; Intracellular Signaling Peptides and Proteins/genetics/metabolism; Male; Middle Aged; Peptic Ulcer/genetics/pathology
- From:The Korean Journal of Gastroenterology 2012;60(2):79-85
- CountryRepublic of Korea
- Language:Korean
- Abstract: BACKGROUND/AIMS: DNA double strand breaks (DSB) is one of the critical types of DNA damage. If unrepaired, DSB is accumulated in the nucleus of cells, the cells become apoptotic or transform to tumor by way of genomic instability. Some of malignant cancers and its premalignant lesions were proven to have DSB in their nuclei. There was no report that Helicobacter pylori (H. pylori), the gastric carcinogen, induce DNA DSB in gastric epithelium in vivo. The aim of this study was to investigate whether H. pylori induce DSB in the gastric epithelial cells of chronic gastritis. METHODS: Immunohistochemical stains were performed for the DSB markers, phospho-53BP1 and gammaH2AX, in the gastric epithelium derived from 44 peptic ulcer disease patients before and after H. pylori eradication. DNA fragmentation assay was performed in the cell line to investigate the DNA damage by H. pylori infection. RESULTS: The mean expression score of gammaH2AX was significantly higher in the H. pylori infected gastric epithelium as compared to the H. pylori eradicated gastric epithelium (8.8+/-5.5 vs. 6.2+/-5.3 respectively; p=0.008). The expression score of phospho-53BP1 between before and after eradication of H. pylori was not statistically different, but tended to be higher in H. pylori infection. DNA fragmentation was developed significantly more in the cell lines after infection with H. pylori. CONCLUSIONS: DSB of DNA damage was typical feature of H. pylori infection in the gastric epithelium.
