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Chang, Byun, Kim, Cho, Kim, Kim, Kim, and Jung: DNA Double Strand Breaks in Gastric Epithelium with Helicobacter pylori Infection
Original Article
Alimentary Tract
The Korean Journal of Gastroenterology

The Korean Journal of Gastroenterology 2012; 60(2): 79-85.

Published online: 22 August 2012

DOI: https://doi.org/10.4166/kjg.2012.60.2.79

DNA Double Strand Breaks in Gastric Epithelium with Helicobacter pylori Infection

Young Jun Chang, Sang Won Byun, Hyung Keun Kim, Young Seok Cho, Sung Soo Kim, Jin Il Kim, Jae Kwang Kim, Eun Sun Jung1

Department of Internal Medicine, The Catholic University of Korea College of Medicine, Seoul, Korea.

1Department of Pathology, The Catholic University of Korea College of Medicine, Seoul, Korea.

Correspondence to: Sung Soo Kim, Department of Internal Medicine, The Catholic University of Korea Uijongbu St. Mary's Hospital, 271 Cheonbo-ro, Uijeongbu 480-717, Korea. Tel: +82-31-820-3000, Fax: +82-31-847-2719, kimss@catholic.ac.kr

Received 15 March 2012       Revised 13 April 2012       Accepted 13 April 2012

Copyright © 2012 The Korean Society of Gastroenterology

(open-access):

This is an open access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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 γH2AX, 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 γH2AX 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.

Keywords: Gastric mucosa, Helicobacter pylori, DNA breaks, double stranded, Gamma-H2AX protein, human, 53BP1 protein, human

Figures and Tables

Fig. 1
Immunohistochemistry for γH2AX and phospho-53BP1 proteins were detected in the nuclei of epithelial and interstitial inflammatory cells of the gastric mucosa (×200). (A) γH2AX before Helicobacter pylori (H. pylori) eradication. (B) γH2AX after eradication. (C) Phospho-53BP1 before eradication. (D) Phospho-53BP1 after eradication. Expression of γH2AX reduced in gastric epithelial cells after the eradication of H. pylori and phospho-53BP1 tended to be decreased after H. pylori eradication.
kjg-60-79-g001
Fig. 2
Change of γH2AX and phospho-53BP1 expressions in the gastric epithelial cells of 44 patients following eradication of Helicobacter pylori (H. pylori). (A) The percentage of epithelial cells expressing γH2AX reduced significantly after eradication of H. pylori. (B) Gastric epithelial cells expressing phospho-53BP1 tended to be decreased after H. pylori eradication. The thick black bars indicate the mean values (**p<0.01). Hp, H. pylori.
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Fig. 3
The induction of DNA fragmentation in Helicobacter pylori (H. pylori) infected AGS cells. Lane 2 and lane 3 in which H. pylori were infected induced DNA fragmentation in cells. Lane 1 indicated AGS, lane 2 was HS3C, lane 3 was AGS infected by H. pylori, and lane 4 was H. pylori only. M indicates molecular marker.
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Table 1
Mean Expression Score of γH2AX and Phospho-53BP1 before and after Helicobacter pylori Eradication
kjg-60-79-i001

Values are presented as mean±SD.

Notes

Financial support: This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2010-0024303).

Conflict of interest: None.

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