Hepcidin-synthesis was reported to be stimulated by
inflammation. In contrast,
hepcidin synthesis was inhibited by TNFα and serum
hepcidin was low. To elucidate these contradictions, we compare data on
hepcidin expression, on
iron absorption and homoeostasis and markers of
inflammation between two murine models of intestinal
inflammation and corresponding wild-types as determined by standard methods. In TNF(ΔARE/+) and IL-10(-/-)-mice hepatic
hepcidin expression and
protein content was significantly lower than in corresponding wild-types. However, (59)Fe whole-body retention showed no difference between knock-outs and corresponding wild-types 7d after gavage, in neither strain. Compared to wild-types,
body weight, hepatic non-
haem iron content,
hemoglobin and hematocrit were significantly decreased in TNF(ΔARE/+) mice, while erythropoiesis increased. These differences were not seen in IL-10(-/-) mice. Duodenal
IL-6 and TNFα content increased significantly in TNF(ΔARE/+) mice, while
ferritin-H decreased along with hepatic
hepcidin expression,
ferritin L, and non-
haem iron. In IL-10(-/-) mice, these changes were less marked or missing for non-
haem iron. Duodenal
ferritin-L and
ferroportin increased significantly, while HFE decreased. 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.