Abstract:
: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.
journal_name
Cell Death Disjournal_title
Cell death & diseaseauthors
Teng Y,Cang B,Mao F,Chen W,Cheng P,Peng L,Luo P,Lu D,You N,Zou Q,Zhuang Ydoi
10.1038/s41419-020-2705-8subject
Has Abstractpub_date
2020-07-01 00:00:00pages
498issue
7issn
2041-4889pii
10.1038/s41419-020-2705-8journal_volume
11pub_type
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