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The Effect of Helicobacter pylori Infection and Dietary Iron Deficiency on Host Iron Homeostasis: A Study in Mice
Author(s) -
Keenan J. I.,
Peterson R. A.,
Fraser R.,
Frampton C. M.,
Walmsley T. A.,
Allardyce R. A.,
Roake J. A.
Publication year - 2004
Publication title -
helicobacter
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.206
H-Index - 79
eISSN - 1523-5378
pISSN - 1083-4389
DOI - 10.1111/j.1083-4389.2004.00278.x
Subject(s) - iron homeostasis , helicobacter pylori , host (biology) , iron deficiency , homeostasis , helicobacter pylori infection , biology , microbiology and biotechnology , immunology , medicine , genetics , endocrinology , gene , anemia
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.