Department of Internal Medicine and Liver Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Gut Liver. 2007 Jun;1(1):40-8. doi: 10.5009/gnl.2007.1.1.40. Epub 2007 Jun 30.
BACKGROUND/AIMS: Interactions between H. pylori and gastric epithelial cells contribute to gastric inflammation and epithelial damage. This study was performed to evaluate the gene expression profile of AGS cells by adhesion of H. pylori.
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.
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.
Host genes are significantly changed by H. pylori adhesion, which might explain the gastroduodenal pathogenesis induced by H. pylori infection.
背景/目的：幽门螺杆菌（H. pylori）与胃上皮细胞的相互作用导致胃炎症和上皮损伤。本研究旨在通过 H. pylori 黏附评估 AGS 细胞的基因表达谱。
通过寡核苷酸微阵列监测共培养（4、12、24、48 小时）时 H. pylori（G69a 株）诱导的 AGS 细胞基因表达变化。采用 Assay-on-Demand Gene Expression 产品方法进行实时逆转录-聚合酶链反应（RT-PCR）验证数据。
H. pylori 黏附使 AGS 细胞中共有 270 个（2.66%）和 19 个基因（0.19%）上调。基因本体论分析表明，上调基因被分为内切脂酶活性（17 个基因）、受体结合（17 个基因）、整合素结合（4 个基因），两个下调基因分为 GTP 结合类别。通过实时 RT-PCR 定量分析 20 个上调和 5 个下调基因的表达水平。涉及细胞因子活性（IL8、IL1B、TNF）、水解酶活性（PTP4A1、ERCC1、CASP8、CASP7、ACIN1）、VIP 受体活性（VIPR2）和神经肽 Y 受体活性（GPR83）的 16 个基因被证实上调。ARF3、M17S2、DDB2、AWP1 和 WTAP 这 5 个基因被证实下调。
宿主基因受 H. pylori 黏附显著改变，这可能解释了 H. pylori 感染引起的胃十二指肠发病机制。
