[2] It leads to the production of three types of mature granulocytes: neutrophils (most abundant, making up to 60% of all white blood cells), eosinophils (up to 4%) and basophils (up to 1%).
[15] Emergency granulopoiesis is a fundamental hematopoietic mechanism activated during acute infections or inflammatory conditions, leading to a swift increase in granulocyte production, especially neutrophils, in the bone marrow.
This process is essential for enhancing the innate immune system's capability to confront pathogen invasions effectively.
However, after a major insult, typically a bacterial infection, the hematopoietic program switches from steady-state to emergency granulopoiesis.
[20][14] The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) is a critical regulator in this context, significantly influencing granulocyte lineage commitment and proliferation, especially noted during candidemia-induced scenarios.
[18] Neutrophils, as primary effector cells of the innate immune defense, originate from HSCs through a series of differentiation stages.
The emergency granulopoiesis significantly accelerates this differentiation process, ensuring a rapid replenishment of neutrophil populations in response to systemic inflammatory stimuli, thus maintaining immune homeostasis.
[23] The clinical significance of understanding emergency granulopoiesis extends beyond basic science, influencing therapeutic strategies against infectious diseases and immune deficiencies.
Balancing rapid neutrophil mobilization against the risk of immune dysregulation is critical, as imbalances can lead to severe conditions like acute respiratory distress syndrome and sepsis-induced organ dysfunctions.