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Curcumin is a potential natural remedy for preventing  Helicobacter pylori -associated gastric inflammation and cancer. Here, we analyzed the effect of a phospholipid formulation of curcumin on  H. pylori  growth, translocation and phosphorylation of the virulence factor CagA and host protein kinase Src  in vitro  and in an  in vivo  mouse model of  H. pylori  infection. Growth of  H. pylori  was inhibited dose-dependently by curcumin  in vitro .  H. pylori  was unable to metabolically reduce curcumin, whereas two enterobacteria,  E. coli  and  Citrobacter rodentium , which efficiently reduced curcumin to the tetra- and hexahydro metabolites, evaded growth inhibition. Oxidative metabolism of curcumin was required for the growth inhibition of  H. pylori  and the translocation and phosphorylation of CagA and cSrc, since acetal- and diacetal-curcumin that do not undergo oxidative transformation were ineffective. Curcumin attenuated mRNA expression of the  H. pylori  virulence genes  cagE  and  cagF  in a dose-dependent manner and inhibited translocation and phosphorylation of CagA in gastric epithelial cells.  H. pylori  strains isolated from dietary curcumin-treated mice showed attenuated ability to induce cSrc phosphorylation and the mRNA expression of the gene encoding for IL-8, suggesting long-lasting effects of curcumin on the virulence of  H. pylori . Our work provides mechanistic evidence that encourages testing of curcumin as a dietary approach to inhibit the virulence of CagA.

Curcumin Oxidation Is Required for Inhibition of Helicobacter pylori Growth, Translocation and Phosphorylation of Cag A