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G-CSF-Induced Emergency Granulopoiesis Modulates Neutrophil Effector Function in Mice.

Jonah K Stephan1, Taylor Knerr1, Collin K Wells1

  • 1Center for Cardiometabolic Science, Christina Lee Brown Envirome Institute, University of Louisville School of Medicine, 580 South Preston Street - Rm 204B, Louisville, KY, USA.

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Summary

Emergency granulopoiesis, triggered by G-CSF, produces neutrophils with altered functions. These neutrophils show impaired reactive oxygen species production and NETosis but enhanced elastase secretion and cytokine expression, influencing inflammation.

Keywords:
CytokineG-CSFGranulopoiesisHematopoiesisInflammationNeutrophil

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Neutrophils are key immune responders, with their function programmed during granulopoiesis.
  • Emergency granulopoiesis is activated during severe inflammation to meet increased neutrophil demand.
  • The functional consequences of emergency granulopoiesis on neutrophils are not well understood.

Purpose of the Study:

  • To investigate the functional impact of emergency granulopoiesis on neutrophils.
  • To assess how neutrophils generated through emergency granulopoiesis influence inflammatory responses in vivo.

Main Methods:

  • Mice were treated with G-CSF to induce emergency granulopoiesis.
  • Neutrophil functions including ROS production, NETosis, elastase secretion, and cytokine expression were assessed.
  • An in vivo model of zymosan-induced peritonitis was used to evaluate the inflammatory response in G-CSF treated mice.

Main Results:

  • Neutrophils from G-CSF treated mice exhibited impaired ROS production and NETosis.
  • These neutrophils showed increased neutrophil elastase secretion and elevated expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-1α, IL-12α, CCL2).
  • In vivo, G-CSF treated mice challenged with zymosan showed increased peritoneal neutrophil CCL2 expression and enhanced macrophage accumulation.

Conclusions:

  • Emergency granulopoiesis reprograms neutrophils, leading to an enhanced immunomodulatory function.
  • These neutrophils play a critical role in orchestrating the subsequent macrophage response during local tissue inflammation.