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Membrane fluidity changes accompanying phagocytosis in normal and in chronic granulomatous disease polymorphonuclear

Blood
|October 1, 1981
PubMed

Insights

Polymorphonuclear leukocytes (PMN) membrane fluidity remains unchanged in chronic granulomatous disease (CGD) patients at rest. During phagocytosis, reactive oxygen species, particularly hydrogen peroxide (H2O2), alter PMN membrane biophysical properties.

Area of Science:

  • Biophysics
  • Cell Biology
  • Immunology

Background:

  • Polymorphonuclear leukocytes (PMN) are crucial immune cells involved in phagocytosis.
  • Membrane fluidity plays a role in cellular functions, including phagocytosis.
  • Chronic granulomatous disease (CGD) is a genetic disorder affecting phagocyte function.

Purpose of the Study:

  • To investigate changes in PMN membrane fluidity during phagocytosis.
  • To determine the role of reactive oxygen species (ROS) in modulating PMN membrane fluidity.
  • To compare membrane fluidity between normal and CGD PMN during phagocytosis.

Main Methods:

  • Electron spin resonance (ESR) spectroscopy using a spin probe (5DS) to assess membrane fluidity via the order parameter (S).
  • Incubation of PMN from normal subjects and CGD patients with opsonized zymosan.
  • Treatment of PMN with ROS scavengers (catalase, superoxide dismutase, sodium benzoate) and glucose oxidase.

Main Results:

  • Resting PMN from normal and CGD subjects showed no significant difference in membrane fluidity (S values).
  • Normal PMN exhibited a significant increase in membrane order (decreased fluidity) upon zymosan stimulation, while CGD PMN did not.
  • ROS scavengers and catalase treatment in normal PMN mimicked the resting state, indicating H2O2's role in fluidity changes.
  • Glucose oxidase-induced H2O2 production in CGD PMN led to altered membrane fluidity.

Conclusions:

  • Reduced oxygen (O2) by-products, especially hydrogen peroxide (H2O2), significantly alter PMN membrane biophysical properties during phagocytosis.
  • CGD, characterized by a defect in ROS production, shows impaired changes in membrane fluidity during phagocytosis.
  • These findings highlight the critical role of ROS in modulating immune cell membrane dynamics.

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