The lining of the stomach is a tight monolayer of epithelial cells performing functions in digestion and a protective barrier against gastric acid, toxic metabolites and infectious agents, including Helicobacter pylori. The response of the epithelial barrier to infections underlies gastric pathologies, including gastric cancer. H. pylori has the unique capacity to colonise the gastric mucosa while evading the immune system. The colonised mucosa initiates an inflammatory response to fight the infection and a strong regenerative program to avoid barrier failure and ulceration. This response changes the morphology and cell composition of the gastric epithelium and in parallel it might contribute to the accumulation of somatic mutations leading to cellular transformation. Genetically modified mice, cell lines and human-derived organoids are the main biological models to study the gastric epithelial barrier. With these models it is possible to dissect the stepwise process of tissue adaptation to infection that places the epithelium at risk of malignant transformation.

胃壁是上皮细胞的紧密单层，在消化中发挥功能，并具有抵抗胃酸，有毒代谢产物和包括幽门螺杆菌在内的传染性物质的保护性屏障。上皮屏障对感染的反应是包括胃癌在内的胃病的基础。幽门螺杆菌具有在逃避免疫系统的同时在胃粘膜上定殖的独特能力。定殖的粘膜可引发炎症反应以抵抗感染，并具有强大的再生程序，可避免屏障衰竭和溃疡。这种反应改变了胃上皮细胞的形态和细胞组成，与此同时，它可能促进了导致细胞转化的体细胞突变的积累。转基因小鼠，细胞系和人类来源的类器官是研究胃上皮屏障的主要生物学模型。使用这些模型，可以剖析组织适应感染的逐步过程，从而使上皮处于恶性转化的风险中。