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Critical role for PI3Kγ-dependent neutrophil reactive oxygen species in WKYMVm-induced microvascular

Li Hao1, Xi Lei1, Hong Zhou2

  • 1Department of Anatomy, Physiology and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Saskatchewan, Canada.

Journal of Leukocyte Biology
|June 20, 2019
PubMed

Insights

Phosphoinositide 3-kinase gamma (PI3Kγ) drives neutrophil-mediated microvascular leakage during acute inflammation by generating reactive oxygen species (ROS). This PI3Kγ-dependent ROS generation is key to formyl peptide-induced hyperpermeability.

Area of Science:

  • Immunology
  • Cell Biology
  • Physiology

Background:

  • Phosphoinositide 3-kinase (PI3K) pathways regulate microvascular permeability.
  • The specific role of PI3K isoforms in neutrophil-driven microvascular leakage during acute inflammation is not fully understood.

Purpose of the Study:

  • To investigate the roles of PI3Kγ and PI3Kδ in formyl peptide (WKYMVm) and chemokine (CXCL2)-induced microvascular permeability.
  • To elucidate the mechanisms underlying PI3K-mediated neutrophil recruitment and microvascular leakage.

Main Methods:

  • Intravital microscopy in mice to assess microvascular permeability, neutrophil adhesion, and emigration.
  • Use of PI3K transgenic mouse strains, chimeric mice, and neutrophil depletion models.
  • Analysis of reactive oxygen species (ROS) generation in neutrophils.

Main Results:

  • PI3Kγ, but not PI3Kδ, mediates WKYMVm-induced microvascular hyperpermeability.
  • This hyperpermeability is neutrophil-dependent and linked to PI3Kγ-mediated ROS generation.
  • Scavenging PI3Kγ-dependent ROS alleviated WKYMVm-induced microvascular leakage.

Conclusions:

  • PI3Kγ plays a critical role in formyl peptide-induced microvascular hyperpermeability.
  • Neutrophil-derived ROS, regulated by PI3Kγ, are essential mediators of this process.
  • Findings highlight PI3Kγ as a potential therapeutic target for inflammatory conditions involving microvascular leakage.
Keywords:
WKYMVmmicrovascular permeabilityneutrophilsphosphatidylinositol 3-kinasereactive oxygen species

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