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Helicobacter pylori -induced inflammation is the strongest known risk factor for gastric adenocarcinoma. Hypoxia-inducible factor-1 (HIF-1α) is a key transcriptional regulator of immunity and carcinogenesis. To examine the role of this mediator within the context of  H. pylori -induced injury, we first demonstrated that HIF-1α levels were significantly increased in parallel with the severity of gastric lesions in humans. In interventional studies targeting HIF-1α,  H. pylori -infected mice were treated ± dimethyloxalylglycine (DMOG), a prolyl hydroxylase inhibitor that stabilizes HIF-1α.  H. pylori  significantly increased proinflammatory chemokines/cytokines and inflammation in vehicle-treated mice; however, this was significantly attenuated in DMOG-treated mice. DMOG treatment also significantly decreased function of the  H. pylori  type IV secretion system (T4SS)  in vivo  and significantly reduced T4SS-mediated NF-κB activation and IL-8 induction  in vitro . These results suggest that prolyl hydroxylase inhibition protects against  H. pylori -mediated pathologic responses, and is mediated, in part, via attenuation of  H. pylori cag -mediated virulence and suppression of host proinflammatory responses.

gut microbes

Targeting hypoxia-inducible factor-1 alpha suppresses  Helicobacter pylori -induced gastric injury via attenuation of both  cag -mediated microbial virulence and proinflammatory host responses