Key Laboratory for Food Microbial Technology of Zhejiang Province, College of Food Science and Biotechnology, Zhejiang Gongshang University, Hangzhou, China.
Helicobacter. 2023 Dec;28(6):e13024. doi: 10.1111/hel.13024. Epub 2023 Oct 5.
Helicobacter pylori (H. pylori) is a highly successful human pathogen that colonizes stomach in around 50% of the global population. The colonization of bacterium induces an inflammatory response and a substantial rise in the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), mostly derived from host neutrophils and gastric epithelial cells, which play a crucial role in combating bacterial infections. However, H. pylori has developed various strategies to quench the deleterious effects of ROS, including the production of antioxidant enzymes, antioxidant proteins as well as blocking the generation of oxidants. The host's inability to eliminate H. pylori infection results in persistent ROS production. Notably, excessive ROS can disrupt the intracellular signal transduction and biological processes of the host, incurring chronic inflammation and cellular damage, such as DNA damage, lipid peroxidation, and protein oxidation. Markedly, the sustained inflammatory response and oxidative stress during H. pylori infection are major risk factor for gastric carcinogenesis. In this context, we summarize the literature on H. pylori infection-induced ROS production, the strategies used by H. pylori to counteract the host response, and subsequent host damage and gastric carcinogenesis.
幽门螺杆菌（H. pylori）是一种高度成功的人类病原体，在全球约 50%的人口中定植于胃部。细菌定植会引发炎症反应，并大量增加活性氧（ROS）和活性氮（RNS）的产生，这些物质主要来自宿主中性粒细胞和胃上皮细胞，它们在抵御细菌感染中发挥着至关重要的作用。然而，H. pylori 已经发展出各种策略来抑制 ROS 的有害影响，包括产生抗氧化酶、抗氧化蛋白以及阻断氧化剂的生成。宿主无法消除 H. pylori 感染会导致持续的 ROS 产生。值得注意的是，过量的 ROS 会破坏宿主的细胞内信号转导和生物过程，导致慢性炎症和细胞损伤，如 DNA 损伤、脂质过氧化和蛋白质氧化。值得注意的是，H. pylori 感染期间持续的炎症反应和氧化应激是导致胃癌发生的主要危险因素。在这种情况下，我们总结了有关 H. pylori 感染诱导的 ROS 产生、H. pylori 对抗宿主反应以及随后的宿主损伤和胃癌发生的文献。
