Expression of ETS1 in gastric epithelial cells positively regulate inflammatory response inHelicobacter pylori-associated gastritis

Gastric epithelial cells (GECs) provide the first point of contact of the host byHelicobacter pylori(H. pylori), and the interaction betweenH. pyloriand GECs plays a critical role inH. pylori-associated diseases. Aberrant expression of transcription factors (TFs) contributes to the pathogenesis of inflammatory disorders, includingH. 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 inH. pylori-infected mouse and human GECs and found that ETS1 (ETS proto-oncogene 1, transcription factor) expression was highly affected byH. pyloriinfection. Then, we reported that ETS1 was induced in GECs byH. pyloriviacagAactivated NF-kappa B pathway. Notably, we demonstrated that proinflammatory cytokines IL-1 beta and TNF alpha have synergistic effects on ETS1 expression duringH. pyloriinfection in an NF-kappa B-pathway-dependent manner. RNA-seq assay and Gene-ontology functional analysis revealed that ETS1 positively regulate inflammatory response duringH. pyloriinfection. Increased ETS1 is also detected in the gastric mucosa of mice and patients withH. pyloriinfection. Collectively, these data showed that ETS1 may play an important role in the pathogenesis ofH. pylori-associated gastritis.