Activated polymorphonuclear leukocytes enhance production of leukocyte microparticles with increased adhesion

Satoshi Fujimi1, Hiroshi Ogura, Hiroshi Tanaka

  • 1Department of Traumatology, Osaka University Medical School, Osaka, Japan. fujimi@hp-emerg.med.osaka-u.ac.jp

The Journal of Trauma
|March 20, 2002
PubMed
Abstract

Insights

Sepsis patients show increased leukocyte microparticles (MPs) with enhanced adhesion molecules. These activated MPs may contribute to sepsis-related endothelial activation and leukocyte-endothelium interactions.

Area of Science:

  • Immunology
  • Pathophysiology
  • Critical Care Medicine

Background:

  • Leukocyte microparticles (MPs) from polymorphonuclear leukocytes (PMNLs) activate vascular endothelium in vitro.
  • The role of leukocyte MPs in severe insults like sepsis is not fully understood.
  • This study investigates leukocyte MP production and adhesion molecule expression in sepsis patients.

Purpose of the Study:

  • To evaluate leukocyte microparticle production in sepsis patients.
  • To assess the expression of adhesion molecules on leukocyte MPs in sepsis.
  • To investigate the relationship between PMNL oxidative activity and MP generation in sepsis.

Main Methods:

  • Flow cytometry was used to measure leukocyte MPs, CD11b expression on MPs, and PMNL oxidative activity.
  • CD11b expression was analyzed based on MP size (<1.0 microm).
  • Soluble E-selectin, thrombomodulin, and PMNL elastase were measured in blood samples.

Main Results:

  • Leukocyte MP production and PMNL superoxide production were significantly higher in sepsis patients compared to controls.
  • CD11b expression was markedly enhanced on smaller MPs (<1.0 microm) in sepsis patients.
  • Increased levels of soluble E-selectin, thrombomodulin, and PMNL elastase were observed in sepsis patients.

Conclusions:

  • Activated PMNLs increase the production of leukocyte MPs with elevated adhesion molecules in sepsis.
  • Activated leukocyte MPs are implicated in the pathogenesis of endothelial activation and leukocyte-endothelium interactions during sepsis.

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