Dexamethasone inhibits apoptosis of human neutrophils induced by reactive oxygen species

Inflammation. 2002 Oct;26(5):215-22. doi: 10.1023/a:1019714618068.


Neutrophils are completely differentiated cells that die in tissues a few days after they migrate from the vascular compartment as a consequence of a rigouous apoptotic program. Many of the mediators produced during an inflammatory response delay neutrophil apoptosis allowing a more efficient removal of microorganisms but also favoring the tissue damage by reactive oxygen species (ROS) and lysosomal proteins released by neutrophils. Glucocorticoids delay the apoptosis of neutrophils but the mechanisms are not completely understood. To investigate the inhibition of glucocorticoids on neutrophil apoptosis we have used the glucose/glucose oxidase (G/GO) system as a constant source of hydrogen peroxide. When neutrophils are incubated in the presence of the G/GO system, a significant acceleration of their apoptotic response is observed. Preincubation with 10(-6) M, 10(-7) M, 10(-8) M or 10(-9) M of dexamethasone, negatively modulated the spontaneous and G/GO induced apoptosis of neutrophils. Then the G/GO system is a useful model to simulate the oxidative stress of neutrophils, and that the effect of DXM on neutrophil apoptosis depends, at least in part, on blocking the proapoptotic effect of ROS.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects*
  • Dexamethasone / pharmacology*
  • Dose-Response Relationship, Drug
  • Drug Antagonism
  • Glucose / metabolism
  • Glucose Oxidase / metabolism
  • Humans
  • Hydrogen Peroxide / pharmacology
  • Neutrophils / cytology*
  • Neutrophils / drug effects
  • Reactive Oxygen Species / pharmacology*


  • Reactive Oxygen Species
  • Dexamethasone
  • Hydrogen Peroxide
  • Glucose Oxidase
  • Glucose