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PTH-065 To define and refine: host iron parameters in a mouse model of Helicobacter infection
  1. M J Thomson1,
  2. S A Boxall2,
  3. J E Crabtree2
  1. 1Department of Molecular Gastroenterology, Leeds Institute of Molecular Medicine, Leeds, UK
  2. 2Molecular Gastroenterology, Leeds Institute for Molecular Medicine, Leeds, UK


Introduction 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. Rodent models of Helicobacter infection need to be refined to investigate any causal links to ID. The aim of this study is to examine haematological parameters during the acute phase of Helicobacter infection in mice fed on iron-replete and iron deficient diets.

Methods Five-week-old female SPF C57Bl/6 mice were fed on iron deficient (2–6 ppm) or iron-replete (48 ppm) diets 3 weeks before oral gavage with H felis. Infected mice and uninfected controls were sacrificed at 4 and 8 weeks post-inoculation. H felis infection was confirmed by urease test and histology. Blood was collected and haematological data were assessed by automated counting machine.

Results Red blood cell count (RBC) and mean corpuscular haemoglobin concentration were similar in groups on both diets regardless of H felis status at 4 and 8 weeks. In uninfected mice total haemoglobin levels were significantly decreased in iron deficient mice at 4 (p<0.01) and 8 weeks (p=0.05). This decrease was abrogated by H felis infection in dietary replete groups due to a slight increase (NS) in haemoglobin. A dichotomy emerges between iron deficient and replete groups for parameters which reflect size and haemoglobin content of erythrocytes. The haematocrit test, mean corpuscular volume (MCV) and mean haemoglobin concentration (MHC) were significantly decreased (p<0.001) in H felis infected and control mice on iron deficient diet compared to matched groups fed on iron-replete diet. A significant increase (p<0.01) in red cell distribution width (RDW) in iron deficiency suggests erythrocytes have an increased variation in cell volume. H felis infection made no difference to the levels observed. White blood cell (WBC) counts were significantly increased at 4 weeks (p<0.03) and 8 weeks (p<0.001) in mice fed on iron defiecient diet, regardless of H felis status.

Conclusion Iron deficiency in this mouse model results in reduced MCH indicating an increased percentage of hypochromic red cells and reduced MCV indicating microcytosis. Increased WBC counts as a result of ID, suggests a higher susceptibility to the effects of inflammation and infection. All other parameters measured showed no difference due to H felis status in either diet cohort. This suggests that H felis has no impact on haematological parameters of iron status in the acute stage of the infection. Other markers of iron status such as serum iron, TIBC and serum ferritin are needed to explore further the impact of Helicobacter infection.

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