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首页> 外文期刊>Infection and immunity >Helicobacter pylori Infection Introduces DNA Double-Strand Breaks in Host Cells
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Helicobacter pylori Infection Introduces DNA Double-Strand Breaks in Host Cells

机译：幽门螺杆菌感染在宿主细胞中引入DNA双链断裂

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摘要

Gastric cancer is an inflammation-related malignancy related to long-standing acute and chronic inflammation caused by infection with the human bacterial pathogen Helicobacter pylori. Inflammation can result in genomic instability. However, there are considerable data that H. pylori itself can also produce genomic instability both directly and through epigenetic pathways. Overall, the mechanisms of H. pylori-induced host genomic instabilities remain poorly understood. We used microarray screening of H. pylori-infected human gastric biopsy specimens to identify candidate genes involved in H. pylori-induced host genomic instabilities. We found upregulation of ATM expression in vivo in gastric mucosal cells infected with H. pylori. Using gastric cancer cell lines, we confirmed that the H. pylori-related activation of ATM was due to the accumulation of DNA double-strand breaks (DSBs). DSBs were observed following infection with both cag pathogenicity island (PAI)-positive and -negative strains, but the effect was more robust with cag PAI-positive strains. These results are consistent with the fact that infections with both cag PAI-positive and -negative strains are associated with gastric carcinogenesis, but the risk is higher in individuals infected with cag PAI-positive strains.
机译：胃癌是与炎症相关的恶性肿瘤，与人类细菌病原体幽门螺杆菌感染引起的长期急性和慢性炎症有关。炎症会导致基因组不稳定。但是，有大量数据表明幽门螺杆菌本身也可以直接或通过表观遗传途径产生基因组不稳定性。总体而言，幽门螺杆菌诱导的宿主基因组不稳定性的机制仍然知之甚少。我们使用了幽门螺杆菌感染的人胃活检标本的微阵列筛选，以鉴定参与幽门螺杆菌诱导的宿主基因组不稳定性的候选基因。我们发现感染幽门螺杆菌的胃粘膜细胞中的 ATM 体内表达 上调。使用胃癌细胞系，我们证实了幽门螺杆菌相关的ATM激活是由于DNA双链断裂（DSBs）的积累。在 cag 致病岛（PAI）阳性和阴性菌株感染后均观察到DSB，但对于 cag PAI阳性菌株，效果更强。这些结果与以下事实相吻合： cag PAI阳性和阴性菌株的感染均与胃癌发生有关，但感染 cag PAI的个体的风险更高阳性菌株。

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