Short- and long-term alterations of hematopoietic cell lineages in rats with congenital iron deficiency.

Data support that fetal iron delivery is prioritized to hemoglobin in erythrocytes (RBC). Iron deficiency (ID) during pregnancy can cause congenital ID, i.e., low fetal iron acquisition. Because how congenital ID impacts other fetal hematopoietic cell lineages is unknown our pilot study examined this in a rat congenital ID model. Pregnant dams fed ID diets were compared to iron sufficient (IS) controls. Iron indices, complete cell counts with differentials, and microscopic morphology were studied at birth P2-3, mid-recovery P15 and adolescent post-recovery P45. Compared to IS at birth, ID rats exhibited 350 % higher zinc protoporphyrin/heme, 70 % lower plasma ferritin, 30 % lower hemoglobin, 25 % fewer platelets, but nucleated RBC (nRBC) and reticulocytes did not differ. Compared to IS at birth, ID rats exhibited 36 % fewer white counts (WBC) but proportionate lymphocytes and granulocytes (all P < 0.015). Compared to IS at P45, RBC, platelets, and WBC numbers did not differ, but lymphocytes were relatively lower in ID (P < 0.01). Microscopic morphology differed from IS in ID, with persistent differences at P45. Because altered inflammatory programming was previously reported in congenital ID and because this pilot study found altered WBC populations, this model of congenital ID is well situated to investigate long-term developmental programming.