The Effect of Helicobacter pylori Infection and Dietary Iron Deficiency on Host Iron Homeostasis: A Study in Mice

ABSTRACT Background. Helicobacter pylori , which requires iron to survive, may cause host iron deficiency by directly competing with the host for available iron or by impairing iron uptake as a consequence of atrophy‐associated gastric hypochlorhydria. The aim of this study was to examine the effect of H. pylori infection and dietary iron deficiency on host iron homeostasis in a mouse model. Materials and Methods. H. pylori SS1‐infected and uninfected C57BL/6 mice, fed either a normal diet or an iron‐deficient diet, were assessed for iron status and infection‐associated gastritis over a 30‐week period. Results. After 10 weeks, serum ferritin values were higher in H. pylori ‐infected mice than in uninfected controls, irrespective of dietary iron intake ( p = .04). The infection‐related increase in body iron stores persisted in the iron‐replete mice but diminished over time in mice with restricted dietary iron intake ( p < .0001). At 30 weeks serum ferritin levels were lower in these animals ( p = .063). No significant difference in bacterial numbers was detected at the 30‐week time point ( p > .05) and the histological changes observed were consistently associated with infection ( p < .01) and not with the iron status of the mice ( p = .771). Conclusions. Infection with H. pylori did not cause iron deficiency in iron‐replete mice. However, diminished iron stores in mice as a result of limited dietary iron intake were further lowered by concurrent infection, thus indicating that H. pylori competes successfully with the host for available iron.