Inflammation neither increases hepatic hepcidin nor affects intestinal 59Fe-absorption in two murine models of bowel inflammation, hemizygous TNFΔARE/+ and homozygous IL-10−/− mice

Our results corroborate the conflicting combination of low hepcidin with inflammation and without increased intestinal iron absorption. Speculating on underlying mechanism, decreased hepcidin may result from stimulated erythropoiesis. Unaltered intestinal iron-absorption may compromise between the stimulation by increased erythropoiesis and inhibition by local and systemic inflammation. The findings suggest intense interaction between counterproductive mechanisms and ask for further research.