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Updated: Aug 11, 2026
Identification and Analysis of Mouse Erythroid Progenitors using the CD71/TER119 Flow-cytometric Assay
Published on: August 5, 2011
Effect of inflammation on erythroid precursors (BFU-E and CFU-E) in bone marrow and spleen of mice
Abstract:
Inflammation, induced in mice by a single intramuscular injection of turpentine, caused a long lasting reduction in the number of morphologically unrecognizable CFU-E in the bone marrow. This resulted in marked decreases in marrow erythroblasts and their iron incorporation into heme. The effect is attributed to blood-borne mediators of inflammation which either caused an emigration of progenitors of CFU-E from the marrow or inhibited their proliferation, possibly as the result of increases in marrow myelopoiesis. CFU-S as well as erythroid and myeloid precursors were markedly increased in the spleen during the inflammatory reaction.
Insights
Inflammation significantly reduced red blood cell precursors (CFU-E) in mouse bone marrow, impacting heme production. This suggests inflammation disrupts normal red blood cell formation through blood-borne mediators.
Area of Science:
- Hematology
- Immunology
- Cell Biology
Background:
- Inflammation is a complex biological response.
- Red blood cell production (erythropoiesis) is crucial for oxygen transport.
- Disruptions in hematopoiesis can lead to anemia and other conditions.
Purpose of the Study:
- To investigate the effects of acute inflammation on erythropoiesis in mice.
- To identify the impact of inflammation on early red blood cell progenitors.
- To understand the mechanisms by which inflammation affects bone marrow cellularity.
Main Methods:
- Induction of inflammation using intramuscular turpentine injection in mice.
- Quantification of colony-forming unit-erythroid (CFU-E) in bone marrow.
- Assessment of erythroblast numbers and heme iron incorporation.
- Analysis of spleen cellularity, including CFU-S, erythroid, and myeloid precursors.
Main Results:
- A long-lasting reduction in morphologically unrecognizable CFU-E was observed in the bone marrow post-inflammation.
- Marked decreases in marrow erythroblasts and their heme iron incorporation occurred.
- Increased CFU-S, erythroid, and myeloid precursors were found in the spleen during inflammation.
- Blood-borne mediators were implicated in CFU-E emigration or proliferation inhibition, potentially due to increased myelopoiesis.
Conclusions:
- Acute inflammation significantly impairs erythropoiesis by reducing CFU-E numbers and function in the bone marrow.
- Inflammation-induced changes in bone marrow myelopoiesis may contribute to erythroid suppression.
- The spleen compensates by increasing hematopoietic precursor populations during inflammatory responses.
