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Regulation of polymorphonuclear leukocyte membrane fluidity: effect of cytoskeletal modification

M E Wiles1, J A Dykens, C D Wright

  • 1Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, Michigan.

Journal of Leukocyte Biology
|August 1, 1994
PubMed

Insights

Cytoskeletal stabilization with phalloidin or taxol reduces polymorphonuclear leukocyte (PMN) membrane fluidity changes during activation. Disrupting cytoskeletons with cytochalasin B or vincristine increases fluidity.

Area of Science:

  • Immunology
  • Cell Biology
  • Biophysics

Background:

  • The f-actin cytoskeleton influences polymorphonuclear leukocyte (PMN) oxidative burst activity.
  • Cytoskeletal elements like actin and microtubules associate with the plasma membrane and PMN NADPH oxidase.

Purpose of the Study:

  • To investigate how cytoskeletal modulation affects PMN membrane fluidity and responses after activation.
  • To determine the role of f-actin and microtubule stabilization or disruption in PMN membrane fluidity.

Main Methods:

  • PMNs were activated with N-formyl-1-methionyl-1-leucyl-1-phenylalanine (fMLP).
  • Membrane fluidity was measured after treatment with agents affecting cytoskeletons: phalloidin/cytochalasin B (f-actin) and taxol/vincristine (microtubules).

Main Results:

  • Phalloidin and taxol decreased PMN membrane fluidity, while cytochalasin B and vincristine increased it.
  • fMLP activation significantly increased membrane fluidity, an effect attenuated by phalloidin or taxol pretreatment.
  • Cytochalasin B and vincristine pretreatment did not alter the fMLP-induced increase in membrane fluidity.

Conclusions:

  • Stabilizing the f-actin or microtubule cytoskeleton can inhibit the increase in PMN membrane fluidity upon activation.
  • Cytoskeletal integrity plays a crucial role in regulating PMN membrane dynamics during inflammatory responses.

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