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Effect of Helicobacter pylori Infection on the Expression of DNA Mismatch Repair Protein
Author(s) -
Park Dong Il,
Park Seung Ha,
Kim Sang Hoon,
Kim Jeong Wook,
Cho Yong Kyun,
Kim Hong Joo,
Sohn Chong Il,
Jeon Woo Kyu,
Kim Byung Ik,
Cho Eun Yoon,
Kim EoJin,
Chae Seoung Wan,
Sohn Jin Hee,
Sung In Kyung,
Sepulveda Antonia R.,
Kim Jae J.
Publication year - 2005
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1523-5378.2005.00309.x
Subject(s) - helicobacter pylori , microsatellite instability , dna mismatch repair , immunohistochemistry , cancer , gastric mucosa , gastritis , staining , medicine , atrophic gastritis , gastroenterology , stomach , chronic gastritis , biology , dna repair , pathology , dna , gene , microsatellite , colorectal cancer , genetics , allele
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.