The data validate the premise that enhanced monocytopoiesis in thermal injury and sepsis results from an imbalance in myelopoiesis that is driven by the increased expression of macrophage colony-stimulating factor receptor.
These data indicate that abrogating PGE2's actions during burn sepsis can restore the balance in bone marrow granulocyte and monocyte production, further consolidating the pivotal role PGE2 plays in the pathogenesis of burn sepsis.
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