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Gut and Liver 2007; 1(1): 040-048 https://doi.org/10.5009/gnl.2007.1.1.40 Analysis of Gene Expression Profile of AGS Cells Stimulated by Helicobacter pylori Adhesion
Author Information
Nayoung Kim*§, Woong-Yang Park†, Jung Mogg Kim‡, Young Soo Park*§, Dong Ho Lee*§, Ji Hyun Park*, Joo Sung Kim*, Hyun Chae Jung*, and In Sung Song*
Departments of *Internal Medicine and Liver Research Institute, and †Biochemistry and Molecular Biology, Seoul National University College of Medicine, Seoul, ‡Department of Microbiology and Institute of Biomedical Science, Hanyang University College of Medicine, Seoul, §Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea

Nayoung Kim
© The Korean Society of Gastroenterology, the Korean Society of Gastrointestinal Endoscopy, the Korean Society of Neurogastroenterology and Motility, Korean College of Helicobacter and Upper Gastrointestinal Research, Korean Association the Study of Intestinal Diseases, the Korean Association for the Study of the Liver, Korean Pancreatobiliary Association, and Korean Society of Gastrointestinal Cancer. All rights reserved.

Abstract
Background/Aims: Interactions between H. pylori and gastric epithelial cells contribute to gastric inflam-mation and epithelial damage. This study was performed to evaluate the gene expression profile of AGS cells by adhesion of H. pylori. Methods: Changes in AGS cell gene expression induced by co-culturing with H. pylori (G69a strain) (4, 12, 24, 48 hours) were monitored using oligonucleotide microarray. Real- time reverse transcription-polymerase chain reaction (RT-PCR) was performed for data validation by the Assay-on-Demand Gene Expression product method. Results: A total of 270 (2.66%) and 19 genes (0.19%) were up-regulated in AGS cells by H. pylori adhesion. Gene ontology analysis showed that up-regulated genes were categorized into endolipidase activity (17 genes), receptor binding (17 genes), integrin binding (4 genes), and two down-regulated genes into GTP binding category. The expression levels of 20 up- and 5 down-regulated genes were quantified by real-time RT-PCR. Sixteen genes involving cytokine activity (IL8, IL1B, TNF), hydrolase activity (PTP4A1, ERCC1, CASP8, CASP7, ACIN1), VIP receptor activity (VIPR2), and neuropeptide Y receptor activity (GPR83) were confirmed to be up-regulated. Five genes, namely, ARF3, M17S2, DDB2, AWP1, and WTAP were confirmed to be down-regulated. Conclusions: Host genes are significantly changed by H. pylori adhesion, which might explain the gastroduodenal pathogenesis induced by H. pylori infection. (Gut and Liver 2007;1:40-48)
Keywords: Helicobacter pylori; Host cell; Adhesion; Microarray
Abstract
Background/Aims: Interactions between H. pylori and gastric epithelial cells contribute to gastric inflam-mation and epithelial damage. This study was performed to evaluate the gene expression profile of AGS cells by adhesion of H. pylori. Methods: Changes in AGS cell gene expression induced by co-culturing with H. pylori (G69a strain) (4, 12, 24, 48 hours) were monitored using oligonucleotide microarray. Real- time reverse transcription-polymerase chain reaction (RT-PCR) was performed for data validation by the Assay-on-Demand Gene Expression product method. Results: A total of 270 (2.66%) and 19 genes (0.19%) were up-regulated in AGS cells by H. pylori adhesion. Gene ontology analysis showed that up-regulated genes were categorized into endolipidase activity (17 genes), receptor binding (17 genes), integrin binding (4 genes), and two down-regulated genes into GTP binding category. The expression levels of 20 up- and 5 down-regulated genes were quantified by real-time RT-PCR. Sixteen genes involving cytokine activity (IL8, IL1B, TNF), hydrolase activity (PTP4A1, ERCC1, CASP8, CASP7, ACIN1), VIP receptor activity (VIPR2), and neuropeptide Y receptor activity (GPR83) were confirmed to be up-regulated. Five genes, namely, ARF3, M17S2, DDB2, AWP1, and WTAP were confirmed to be down-regulated. Conclusions: Host genes are significantly changed by H. pylori adhesion, which might explain the gastroduodenal pathogenesis induced by H. pylori infection. (Gut and Liver 2007;1:40-48)
Keywords: Helicobacter pylori; Host cell; Adhesion; Microarray
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