Helicobacter pylori is known to be an etiologic agent of gastritis and
peptic ulcer disease in humans. However, the mechanism by which this
organism acquires iron has not been studied. For this investigation, H
. pylori was grown in iron-restricted medium. Siderophore production w
as not detected by chemical assays, and the strains were unable to use
enterochelin and pyochelin for growth in low-iron media. Human lactof
errin supported full growth of the bacteria in media lacking other iro
n sources, but neither human transferrin, bovine lactoferrin, nor hen
ovotransferrin served as a source for iron. Since lactoferrin was foun
d in significant amounts in human stomach resections with superficial
or atrophic gastritis, the iron acquisition system of H. pylori by the
human lactoferrin receptor system may play a major role in the virule
nce of H. pylori infection.