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Helicobacter pylori  infects half the world's population, and carriage is lifelong without antibiotic therapy. Current regimens prescribed to prevent infection-associated diseases such as gastroduodenal ulcers and gastric cancer can be thwarted by antibiotic resistance. We reported that administration of 1%  d , l -α-difluoromethylornithine (DFMO) to mice infected with  H. pylori  reduces gastritis and colonization, which we attributed to enhanced host immune response due to inhibition of macrophage ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis. Although no ODC has been identified in any  H. pylori  genome, we sought to determine if DFMO has direct effects on the bacterium. We found that DFMO significantly reduced the growth rate of  H. pylori  in a polyamine-independent manner. Two other Gram-negative pathogens possessing ODC,  Escherichia coli  and  Citrobacter rodentium , were resistant to the DFMO effect. The effect of DFMO on  H. pylori  required continuous exposure to the drug and was reversible when removed, with recovery of growth rate  in vitro  and the ability to colonize mice.  H. pylori  exposed to DFMO were significantly shorter in length than those untreated and they contained greater internal levels of ATP, suggesting severe effects on bacterial metabolism. DFMO inhibited expression of the  H. pylori  virulence factor cytotoxin associated gene A, and its translocation and phosphorylation in gastric epithelial cells, which was associated with a reduction in interleukin-8 expression. These findings suggest that DFMO has effects on  H. pylori  that may contribute to its effectiveness in reducing gastritis and colonization and may be a useful addition to anti- H. pylori  therapies.

Difluoromethylornithine Is a Novel Inhibitor of Helicobacter pylori Growth, CagA Translocation, and Interleukin-8 Induction