Normark Staffan, Nilsson Christina, Normark Birgitta Henriques, Hornef Mathias W
Microbiology and Tumor Biology Center and Smittskyddsinstitutet, Karolinska Institutet, Stockholm, Sweden.
Adv Cancer Res. 2003;90:63-89. doi: 10.1016/s0065-230x(03)90002-9.
Gastric malignancies have been closely linked to infection of the gastric mucosa with Helicobacter pylori, but the individual factors involved in the multistage process of tumor development are still poorly understood. H. pylori evades the host defense system and causes persistent infection and chronic inflammation. Immune activation leads to DNA damage by the release of oxygen and nitrogen radicals. Ongoing tissue repair mechanisms and the secretion of cytokines and growth factors, as well as bacterial effector molecules, cause disturbances in the balance between epithelial cell proliferation and apoptosis, promote the accumulation of potential oncogenic mutations, and support neovascularization and tumor growth. In addition, H. pylori might hamper the development of an efficient antitumor immunity and provoke immune-mediated pathology. This review summarizes the recent progress in the understanding of the intimate bacteria-host relationship and the mechanisms by which H. pylori may promote the process of tumor development.
胃恶性肿瘤与幽门螺杆菌感染胃黏膜密切相关，但肿瘤发生多阶段过程中涉及的个体因素仍知之甚少。幽门螺杆菌逃避宿主防御系统，导致持续感染和慢性炎症。免疫激活通过释放氧自由基和氮自由基导致DNA损伤。持续的组织修复机制、细胞因子和生长因子的分泌以及细菌效应分子，会导致上皮细胞增殖与凋亡之间的平衡失调，促进潜在致癌突变的积累，并支持新血管形成和肿瘤生长。此外，幽门螺杆菌可能会阻碍有效的抗肿瘤免疫的发展，并引发免疫介导的病理反应。本综述总结了在理解细菌与宿主密切关系以及幽门螺杆菌促进肿瘤发生过程的机制方面的最新进展。
