Iron deficiency (ID) is the most common nutritional disorder globally. There is increasing evidence from clinical and population studies for a role of H. pylori infection in the aetiology of ID. The role of the Cag pathogenicity island (Cag PAI) in this phenomenon is not well elucidated. Rodent models of gastric Helicobacter infection are needed to investigate any causal links to ID.
The aim of this study is to examine gene expression of the host iron metabolism genes measured in the stomach, liver and duodenum of mice with gastric infections of either H. felis (Cag PAI-) or mouse-adapted human H. pylori SS1 (Cag PAI+). These mice and uninfected litter mate controls were maintained on normal chow until sacrificed 20 weeks post-inoculation by oral gavage. Blood was collected and haematological data assessed by automated counting machine. Tissue was snap frozen in liquid nitrogen and total RNA extracted to make cDNA for semi-quantitative Real Time PCR studies.
Chronic gastric H. felis infection in mice resulted in lower HGB and a significant reduction in MCV and MCH levels when compared to uninfected mice, but no significant haematological changes were observed in the group infected with H. pylori SS1 compared to controls. Both H. felis and H. pylori SS1 infection resulted in significant decreases in gene expression of the global iron regulator, hepcidin, in all tissues tested, most notably the liver, when compared to controls. These results indicate that chronic gastric Helicobacter infection can modulate the expression of host iron metabolism genes, independently of Cag PAI status of the infecting strain.