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Map3k8 controls granulocyte colony-stimulating factor production and neutrophil precursor proliferation in

Ángela Sánchez1, Carlos Relaño1, Araceli Carrasco1

  • 1Instituto de Investigaciones Biomédicas "Alberto Sols" Madrid, Consejo Superior de Investigaciones Científicas (CSIC-UAM), Madrid, Spain.

Scientific Reports
|July 12, 2017
PubMed

Insights

Map3k8 deficiency impairs neutrophil production during emergency granulopoiesis. Map3k8 is crucial for increasing circulating neutrophils and their precursors, impacting G-CSF production and cell proliferation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Map3k8 (Mitogen-activated protein kinase 8) has been investigated as a therapeutic target for inflammatory conditions.
  • Emergency granulopoiesis is a critical response to infection, involving rapid neutrophil production.

Purpose of the Study:

  • To investigate the role of Map3k8 in lipopolysaccharide (LPS)-induced emergency granulopoiesis.
  • To determine the impact of Map3k8 deficiency on neutrophil populations and their precursors.

Main Methods:

  • Utilized Map3k8 knockout (Map3k8-/-) mice and chimeric bone marrow transplantation models.
  • Administered lipopolysaccharide (LPS) to induce emergency granulopoiesis.
  • Analyzed circulating and bone marrow neutrophil populations (Ly6GhighCD11b+ and Ly6GlowCD11b+) via flow cytometry.
  • Measured granulocyte colony-stimulating factor (G-CSF) levels and CCAAT-enhancer-binding protein β (C/EBPβ) expression.
  • Assessed bone marrow cell proliferation.

Main Results:

  • Map3k8 deficiency significantly impaired the increase of both mature (Ly6GhighCD11b+) and immature (Ly6GlowCD11b+) neutrophils during LPS-induced emergency granulopoiesis.
  • LPS-treated Map3k8-/- mice exhibited reduced G-CSF production and impaired expression of C/EBPβ in bone marrow cells.
  • Map3k8 deficiency led to decreased proliferation of immature neutrophils (Ly6GlowCD11b+) in the bone marrow.
  • Map3k8 activity in non-hematopoietic tissues is essential for LPS-induced emergency granulopoiesis.

Conclusions:

  • Map3k8 plays a critical role in regulating emergency granulopoiesis by influencing G-CSF production and subsequent neutrophil precursor proliferation.
  • Inhibition of Map3k8 activity reduces neutrophilia during systemic infection, suggesting potential risks for its use as an anti-inflammatory therapy in such contexts.

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