Gastric epithelial cells (GECs) provide the first point of contact of the host by Helicobacter pylori (H. pylori), and the interaction between H. pylori and GECs plays a critical role in H. pylori-associated diseases. Aberrant expression of transcription factors (TFs) contributes to the pathogenesis of inflammatory disorders, including H. pylori-associated gastritis. ETS (E26 transformation specific) transcription factor family is one of the largest families of evolutionarily conserved TFs, regulating critical functions during cell homeostasis. We screened ETS family gene expression in H. pylori-infected mouse and human GECs and found that ETS1 (ETS proto-oncogene 1, transcription factor) expression was highly affected by H. pylori infection. Then, we reported that ETS1 was induced in GECs by H. pylori via cagA activated NF-κB pathway. Notably, we demonstrated that proinflammatory cytokines IL-1β and TNFα have synergistic effects on ETS1 expression during H. pylori infection in an NF-κB-pathway-dependent manner. RNA-seq assay and Gene-ontology functional analysis revealed that ETS1 positively regulate inflammatory response during H. pylori infection. Increased ETS1 is also detected in the gastric mucosa of mice and patients with H. pylori infection. Collectively, these data showed that ETS1 may play an important role in the pathogenesis of H. pylori-associated gastritis.

胃上皮细胞（GEC）提供了幽门螺杆菌（H. pylori）与宿主的第一接触点，幽门螺杆菌与GEC之间的相互作用在幽门螺杆菌相关疾病中起着至关重要的作用。转录因子（TFs）的异常表达助长了包括幽门螺杆菌相关性胃炎在内的炎性疾病的发病机理。ETS（E26转化特异性）转录因子家族是进化上保守的TF的最大家族之一，可调节细胞稳态过程中的关键功能。我们筛选了幽门螺杆菌中ETS家族基因的表达感染小鼠和人类GEC，发现ETS1（ETS原癌基因1，转录因子）的表达受到幽门螺杆菌感染的高度影响。然后，我们报道了幽门螺杆菌经由cagA激活的NF-κB途径在GEC中诱导ETS1 。值得注意的是，我们证明了幽门螺杆菌感染期间促炎细胞因子IL-1β和TNFα以NF-κB途径依赖性方式协同作用于ETS1表达。RNA序列测定和基因本体功能分析表明，ETS1在幽门螺杆菌感染过程中积极调节炎症反应。在小鼠和幽门螺杆菌患者的胃粘膜中也检测到ETS1增加感染。总的来说，这些数据表明ETS1可能在幽门螺杆菌相关性胃炎的发病机理中起重要作用。