Lansoprazole is a gastric parietal cell proton pump inhibitor that is
also active against Helicobacter pylori in vitro. We aimed to investig
ate further the mechanism of its antimicrobial effect. The antimicrobi
al activity of lansoprazole and of its sulfenamide, a rearrangement pr
oduct occurring spontaneously in acid environments, was studied by det
ermining the MICs and MBCs for II cytotoxic and eight non-cytotoxic ii
. pylori strains and by measuring the rapidity of bacterial killing. T
he MIC90 and MBC90 were 2.5 mg/L and 10 mg/L, respectively, both for l
ansoprazole and for its sulfenamide. Cytotoxic strains were as suscept
ible as noncytotoxic strains. The sulfenamide exhibited faster bacteri
cidal activity. Lansoprazole did not inhibit the toxin-induced vacuoli
zation of HeLa cells by a cytotoxic strain, hence its anti-H. pylori a
ctivity does not depend on inhibition of a v-ATPase-mediated, toxin-in
duced activity. Sulfenamide formation is likely to occur in vivo in th
e gastric environment, thus enhancing the bactericidal activity of the
drug. Lansoprazole is likely to be useful, in association with antibi
otics, in the treatment of H. pylori infection regardless of the cytot
oxicity of the infecting strain.