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Dialysis membrane-induced neutrophil apoptosis is mediated through free radicals

N Nahar1, H Shah, J Siu

  • 1Department of Medicine, Long Island Jewish Medical Center, Albert Einstein College of Medicine, New York, NY 11040, USA.

Clinical Nephrology
|August 14, 2001
PubMed

Insights

Patients undergoing hemodialysis experience increased neutrophil apoptosis, a key immune cell function. Dialysis membranes, particularly cellulose acetate, directly induce this apoptosis, impacting immune defense in dialysis patients.

Area of Science:

  • Immunology
  • Nephrology
  • Biomaterials Science

Background:

  • Patients on hemodialysis are susceptible to infections.
  • Neutrophils are critical for combating microbial pathogens.
  • Neutrophil apoptosis impairs immune function.

Purpose of the Study:

  • To investigate the impact of dialysis membranes on neutrophil apoptosis.
  • To compare the effects of cellulose acetate and polysulfone membranes on neutrophil apoptosis.
  • To elucidate the mechanisms underlying membrane-induced neutrophil apoptosis.

Main Methods:

  • Comparing neutrophil apoptosis in hemodialysis patients versus controls.
  • Exposing neutrophils to cellulose acetate and polysulfone membranes in vitro.
  • Assessing the role of reactive oxygen species (ROS) and nitric oxide synthase (NOS) in apoptosis.
  • Investigating the influence of monocyte-neutrophil interactions.

Main Results:

  • Hemodialysis patients exhibited significantly higher neutrophil apoptosis than controls.
  • Cellulose acetate membranes significantly increased neutrophil apoptosis compared to polysulfone membranes.
  • Reactive oxygen species and nitric oxide contributed to membrane-induced apoptosis.
  • Monocyte-neutrophil interactions exacerbated apoptosis.

Conclusions:

  • Dialysis membranes can directly induce neutrophil apoptosis.
  • Membrane-induced apoptosis is partly mediated by ROS and nitric oxide.
  • Interactions with monocytes further promote neutrophil apoptosis in dialysis patients.
  • These findings highlight a mechanism contributing to compromised immunity in hemodialysis.

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