Liatsos Christos, Papaefthymiou Apostolis, Kyriakos Nikolaos, Galanopoulos Michail, Doulberis Michael, Giakoumis Marios, Petridou Evangelia, Mavrogiannis Christos, Rokkas Theodore, Kountouras Jannis
Department of Gastroenterology, 401 General Military Hospital of Athens, Athens 11525, Greece.
Division of Gastroenterology and Hepatology, Medical University Department, Kantonsspital Aarau, Aarau 1234, Switzerland.
World J Gastrointest Oncol. 2022 May 15;14(5):959-972. doi: 10.4251/wjgo.v14.i5.959.
infection (I) represents a typical microbial agent intervening in the complex mechanisms of gastric homeostasis by disturbing the balance between the host gastric microbiota and mucosa-related factors, leading to inflammatory changes, dysbiosis and eventually gastric cancer. The normal gastric microbiota shows diversity, with [ () belongs to this family], , , and being the most abundant phyla. Most studies indicate that has inhibitory effects on the colonization of other bacteria, harboring a lower diversity of them in the stomach. When comparing the healthy with the diseased stomach, there is a change in the composition of the gastric microbiome with increasing abundance of (where present) in the gastritis stage, while as the gastric carcinogenesis cascade progresses to gastric cancer, the oral and intestinal-type pathogenic microbial strains predominate. I creates a premalignant environment of atrophy and intestinal metaplasia and the subsequent alteration in gastric microbiota seems to play a crucial role in gastric tumorigenesis itself. Successful eradication is suggested to restore gastric microbiota, at least in primary stages. It is more than clear that I, gastric microbiota and gastric cancer constitute a challenging tangle and the strong interaction between them makes it difficult to unroll. Future studies are considered of crucial importance to test the complex interaction on the modulation of the gastric microbiota by as well as on the relationships between the gastric microbiota and gastric carcinogenesis.
感染（I）代表一种典型的微生物因子，它通过扰乱宿主胃微生物群与黏膜相关因子之间的平衡，干预胃内稳态的复杂机制，导致炎症变化、生态失调并最终引发胃癌。正常的胃微生物群具有多样性，[（）属于这个家族]、、、和是最丰富的门类。大多数研究表明，对其他细菌的定殖具有抑制作用，胃中其多样性较低。比较健康胃和患病胃时，胃微生物组的组成会发生变化，在胃炎阶段（如果存在）丰度增加，而随着胃癌发生级联发展为胃癌，口腔型和肠型致病微生物菌株占主导。感染会造成萎缩和肠化生的癌前环境，随后胃微生物群的改变似乎在胃癌发生过程中起关键作用。成功根除感染被认为至少在初期可恢复胃微生物群。很明显，感染、胃微生物群和胃癌构成了一个具有挑战性的难题，它们之间的强烈相互作用使其难以理清。未来的研究对于测试感染对胃微生物群调节的复杂相互作用以及胃微生物群与胃癌发生之间的关系至关重要。
