Effect of Helicobacter pylori Infection on the Expression of DNA Mismatch Repair Protein

幽门螺杆菌 微卫星不稳定性 DNA错配修复 胃炎 免疫组织化学 癌症 胃粘膜 萎缩性胃炎 慢性胃炎 染色 内科学 胃肠病学 DNA修复 医学 生物 病理 DNA 基因 微卫星 结直肠癌 遗传学 等位基因
作者
Dong Il Park,Sungha Park,Sang Hoon Kim,Jeong Wook Kim,Yong Kyun Cho,Hong Joo Kim,Chong Il Sohn,Woo Kyu Jeon,Byung Ik Kim,Eun Yoon Cho,Eo‐Jin Kim,Seoung Wan Chae,Jin Hee Sohn,In Kyung Sung,Antonia R. Sepulveda,Jae J. Kim
出处
期刊:Helicobacter [Wiley]
卷期号:10 (3): 179-184 被引量:55
标识
DOI:10.1111/j.1523-5378.2005.00309.x
摘要

Abstract Background. Helicobacer pylori infection is a major gastric cancer risk factor. Deficient DNA mismatch repair (MMR) caused by H. pylori may underlie microsatellite instability (MSI) in the gastric epithelium and may represent a major mechanism of mutation accumulation in the gastric mucosa during the early stages of H. pylori ‐associated gastric carcinogenesis. In this study, we examined the expression of DNA MMR protein (hMLH1 and hMSH2) in patients with chronic H. pylori infection before and after eradication of the infection. Materials and methods. Gastric tissue samples were collected from 60 patients with H. pylori gastritis and peptic ulcer disease before and after eradication of the infection. The DNA MMR protein expression (hMLH1 and hMSH2) was determined by immunohistochemical staining in 60 patients before and after H. pylori eradication. The percentage of epithelial cell nuclei and intensity of staining were then compared in gastric biopsies before and after eradication. Results. The percentage of hMLH1 (76.60 ± 20.27, 84.82 ± 12.73, p = .01) and hMSH2 (82.36 ± 12.86, 88.11 ± 9.27, p < .05) positive epithelial cells significantly increased in 53 patients who became H. pylori ‐negative after eradication therapy. However, the intensity of hMLH1 and hMSH2 staining was not significantly different. In those 7 patients, who did not respond to the eradication therapy and were still H. pylori ‐positive, the percent positivity and intensity of hMLH1 and hMSH2 staining did not change. Conclusions. The expression of DNA MMR proteins increased in the gastric mucosa after H. pylori eradication, indicating that H. pylori gastritis may be associated with a reduced DNA MMR system during infection. The effect of H. pylori infection on MMR protein expression appears to be at least partially reversible after H. pylori eradication. These data suggest that H. pylori gastritis might lead to a deficiency of DNA MMR in gastric epithelium that may increase the risk of mutation accumulation in the gastric mucosa cells during chronic H. pylori infection.
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