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Human neutrophil-pulmonary microvascular endothelial cell interactions in vitro: differential effects of nitric oxide

Jennifer L Shelton1, Lefeng Wang, Gediminas Cepinskas

  • 1Department of Medicine, Division of Respirology, London Health Sciences Center, Centre for Critical Illness Research, Lawson Health Research Institute University of Western Ontario, London, Ontario Canada.

Microvascular Research
|July 12, 2008
PubMed

Insights

Nitric oxide (NO) inhibits human neutrophil adhesion and migration in sepsis-induced acute lung injury. Peroxynitrite, however, stimulates these interactions, contributing to pulmonary microvascular endothelial cell (PMVEC) barrier dysfunction.

Area of Science:

  • Pulmonary medicine
  • Endothelial cell biology
  • Inflammation research

Background:

  • Sepsis-induced acute lung injury involves pulmonary microvascular endothelial cell (PMVEC) activation and injury.
  • Neutrophil adhesion and migration across PMVECs contribute to lung edema.
  • The role of nitric oxide (NO) in human neutrophil-PMVEC interactions during sepsis is unclear.

Purpose of the Study:

  • To investigate the effects of NO and related reactive nitrogen species on human neutrophil-PMVEC interactions.
  • To determine the impact of these interactions on PMVEC barrier function.

Main Methods:

  • Human PMVECs were isolated and co-cultured with human neutrophils.
  • Neutrophil adhesion, trans-PMVEC migration, and albumin leak were assessed.
  • NO donors, inducible NO synthase (iNOS) inhibition, and peroxynitrite donors were used, with and without scavengers.

Main Results:

  • NO donors attenuated neutrophil-PMVEC adhesion and trans-PMVEC migration.
  • iNOS inhibition enhanced neutrophil migration but not adhesion.
  • Peroxynitrite donor increased both adhesion and migration, effects blocked by scavengers.
  • Neutrophil-PMVEC adhesion, not migration, contributed to PMVEC barrier dysfunction.

Conclusions:

  • NO exerts inhibitory effects on human neutrophil-PMVEC interactions in a sepsis-like model.
  • Peroxynitrite stimulates these interactions, potentially exacerbating lung injury.
  • Neutrophil adhesion to PMVECs is a key factor in sepsis-induced PMVEC barrier dysfunction.

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