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

Area of Science:

• Hematology
• Developmental Biology
• Nutritional Science

Background:

• Fetal iron delivery is primarily directed to red blood cells (RBCs) for hemoglobin synthesis.
• Maternal iron deficiency (ID) during pregnancy can result in congenital ID in the fetus, impairing iron acquisition.
• The impact of congenital ID on fetal hematopoietic cell lineages beyond erythrocytes remains largely unexplored.

Purpose of the Study:

• To investigate the effects of congenital iron deficiency on various fetal hematopoietic cell lineages in a rat model.
• To assess the recovery of hematopoietic parameters following iron repletion in adolescent rats post-congenital ID.
• To evaluate the potential of this congenital ID model for studying long-term developmental programming alterations.

Main Methods:

• A rat model of congenital iron deficiency was established by feeding pregnant dams iron-deficient diets.
• Hematological parameters, including iron indices, complete blood counts with differentials, and cell morphology, were analyzed at birth (P2-3), mid-recovery (P15), and post-recovery (P45).
• Iron-sufficient (IS) control groups were used for comparison throughout the study.

Main Results:

• At birth, ID rats showed significantly elevated zinc protoporphyrin/heme, reduced plasma ferritin and hemoglobin, and decreased platelet counts compared to IS controls.
• White blood cell (WBC) counts were lower in ID rats at birth, with proportionate lymphocyte and granulocyte populations.
• While RBC, platelet, and WBC counts normalized by P45, lymphocytes remained relatively lower in ID rats, and persistent morphological differences were observed.

Conclusions:

• Congenital iron deficiency significantly impacts fetal hematopoiesis, affecting erythrocytes, platelets, and white blood cells.
• Despite apparent recovery in cell counts by adolescence, subtle but persistent alterations in lymphocyte populations and cell morphology suggest long-term programming effects.
• This rat model of congenital ID provides a valuable platform for investigating the lasting consequences of early-life iron deficiency on developmental programming and inflammatory responses.