McNamara D, El-Omar E
Department of Gastroenterology, Aberdeen Royal Infirmary, United Kingdom.
Dig Liver Dis. 2008 Jul;40(7):504-9. doi: 10.1016/j.dld.2008.02.031. Epub 2008 May 16.
Helicobacter pylori infection is the most important acquired risk factor for gastric cancer. The infection initiates a chronic inflammatory process that eventually alters the physiology of the gastric environment and leads to achlorohydria. Gastric atrophy may be part of this process but cancer can arise without this precursor. The net effect of decades of inflammation is the establishment of a milieu awash with pro-inflammatory cytokines and characterized by the activation of signalling pathways that cross-talk between inflammation and carcinogenesis. Many of the factors involved in chronic inflammation play a dual role in the process-promoting neoplastic progression but also facilitating cancer prevention. H. pylori bacterial virulence factors as well as host genetic factors play a major role in orchestrating the increased risk of cancer. The study of such host-bacterial interaction is key to uncovering the molecular and cellular pathways involved and will ultimately lead to developing preventive and therapeutic strategies against this global killer.
幽门螺杆菌感染是胃癌最重要的后天危险因素。这种感染引发慢性炎症过程，最终改变胃环境的生理状况并导致胃酸缺乏。胃萎缩可能是这一过程的一部分，但癌症也可能在没有这种前驱病变的情况下发生。数十年炎症的最终结果是形成了一个充斥着促炎细胞因子的环境，其特征是炎症与致癌作用之间相互作用的信号通路被激活。慢性炎症涉及的许多因素在这一过程中发挥着双重作用——既促进肿瘤进展，也有助于癌症预防。幽门螺杆菌的细菌毒力因子以及宿主遗传因素在协同增加癌症风险方面起着主要作用。对这种宿主 - 细菌相互作用的研究是揭示所涉及的分子和细胞途径的关键，最终将有助于制定针对这种全球杀手的预防和治疗策略。
