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There is increasing evidence from clinical and population studies for a role of  H. pylori  infection in the aetiology of iron deficiency. Rodent models of  Helicobacter  infection are helpful for investigating any causal links and mechanisms of iron deficiency in the host. The aim of this study was to investigate the effects of gastric  Helicobacter  infection on iron deficiency and host iron metabolism/transport gene expression in hypergastrinemic INS-GAS mice. INS-GAS mice were infected with  Helicobacter felis  for 3, 6 and 9 months. At post mortem, blood was taken for assessment of iron status and gastric mucosa for pathology, immunohistology and analysis of gene expression. Chronic  Helicobacter  infection of INS- GAS mice resulted in decreased serum iron, transferrin saturation and hypoferritinemia and increased Total iron binding capacity (TIBC). Decreased serum iron concentrations were associated with a concomitant reduction in the number of parietal cells, strengthening the association between hypochlorhydria and gastric  Helicobacter -induced iron deficiency. Infection with  H. felis  for nine months was associated with decreased gastric expression of iron metabolism regulators hepcidin,  Bmp4  and  Bmp6  but increased expression of Ferroportin 1, the iron efflux protein, iron absorption genes such as Divalent metal transporter 1, Transferrin receptor 1 and also  Lcn2  a siderophore-binding protein. The INS-GAS mouse is therefore a useful model for studying  Helicobacter -induced iron deficiency. Furthermore, the marked changes in expression of gastric iron transporters following  Helicobacter  infection may be relevant to the more rapid development of carcinogenesis in the  Helicobacter  infected INS-GAS model.

Gastric Helicobacter Infection Induces Iron Deficiency in the INS-GAS Mouse