Helicobacter, Inflammation, and Gastric Cancer.
Helicobacter, Inflammation, and Gastric Cancer.
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DOI：
10.1007/s40139-013-0009-8
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发表时间：
2013-03
影响因子：
--
通讯作者：
Sepulveda AR
中科院分区：
文献类型：
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作者：
Sepulveda AR
幽门螺杆菌感染导致长期慢性炎症，是胃癌最常见的危险因素。最近，关于幽门螺杆菌和粘膜炎症导致癌症发展的机制的新见解已经出现。幽门螺杆菌毒力因子，特别是特定的CagA基因型，是胃癌的主要因素，诱导上皮细胞内信号传导的改变。幽门螺杆菌感染的慢性性质似乎与VacA毒力因子和Th17/Treg机制有关。幽门螺杆菌感染在表观遗传和microRNA失调中的作用已被证实。上皮细胞基因组突变是癌症的标志，在幽门螺杆菌感染的胃中积累，部分原因是DNA修复不足。胃干细胞被证明是幽门螺杆菌炎症环境中氧化损伤的目标。本文综述了近年来细菌因子、炎症介质和宿主上皮反应在胃癌发生中的作用。
Helicobacter pylori infection leads to long-lasting chronic inflammation and represents the most common risk factor underlying gastric cancer. Recently, new insights into the mechanisms through which H. pylori and mucosal inflammation lead to cancer development have emerged. H. pylori virulence factors, in particular specific CagA genotypes, represent main factors in gastric cancer, inducing altered intracellular signaling in epithelial cells. The chronic nature of H. pylori infection appears to relate to the VacA virulence factor and Th17/Treg mechanisms. A role of H. pylori infection in epigenetic and microRNA deregulation has been shown. Mutation of the epithelial cell genome, a hallmark of cancer, was demonstrated to accumulate in H. pylori infected stomach partly due to inadequate DNA repair. Gastric stem cells were shown to be targets of oxidative injury in the Helicobacter-inflammatory milieu. Recent advances emphasizing the contribution of bacterial factors, inflammatory mediators, and the host epithelial response in gastric carcinogenesis are reviewed.