Epidemiological data and animal models indicate that Helicobacter pylori and dietary NaCl have a synergistic ill effect on gastric maladies. Here we show that the Ferric Uptake Regulator (Fur), which is a crucial regulatory factor required for H. pylori colonization, is essential for growth in the presence of high NaCl concentrations. Moreover, we demonstrate that the transcriptional response induced by sodium chloride stress exhibits similarities to that seen under iron depletion.