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Effect of cytokines and colony-stimulating factors on passive polymorphonuclear leukocyte deformability in vitro

A T Skoutelis1, V E Kaleridis, C A Gogos

  • 1Section of Infectious Diseases, Patras University Medical School, Patras, Greece. skout@med.upatras.gr

Cytokine
|October 29, 2000
PubMed

Insights

Certain cytokines and colony-stimulating factors (CSFs) directly reduce the deformability of polymorphonuclear leukocytes (PMNs), impacting their function. This study investigated how various immune signaling molecules affect PMN flexibility.

Area of Science:

  • Immunology
  • Cell Biology
  • Hematology

Background:

  • Cytokines are key immune mediators that activate polymorphonuclear leukocytes (PMNs).
  • PMN deformability is crucial for their migration and function during inflammation.
  • Previous research suggests cytokines can alter PMN properties, but direct effects on deformability require further investigation.

Purpose of the Study:

  • To evaluate the direct impact of various cytokines and colony-stimulating factors (CSFs) on passive polymorphonuclear leukocyte (PMN) deformability.
  • To determine the dose-dependent effects of these immune mediators on PMN mechanical properties.
  • To explore potential synergistic effects of combined cytokine treatments on PMN rigidity.

Main Methods:

  • Passive PMN deformability was assessed using the micropipette aspiration technique.
  • PMNs were incubated with varying concentrations of lipopolysaccharide (LPS), interleukins (IL-1, IL-6, IL-8, IL-10), tumor necrosis factor (TNF), granulocyte-CSF (G-CSF), and granulocyte-macrophage-CSF (GM-CSF).
  • The effects of individual and combined treatments on PMN rigidity were measured.

Main Results:

  • Tumor necrosis factor (TNF), IL-1, G-CSF, and GM-CSF significantly decreased PMN deformability in a dose-dependent manner.
  • IL-6 also reduced PMN deformability, though to a lesser extent.
  • Lipopolysaccharide (LPS) did not directly affect PMN deformability.
  • Combinations of cytokines, even at concentrations that had no individual effect, increased PMN rigidity.

Conclusions:

  • Several cytokines and CSFs directly impair PMN deformability, independent of their activation effects.
  • These findings highlight a direct mechanism by which immune signaling molecules can modulate PMN mechanical function.
  • Altered PMN deformability may have significant implications for inflammatory responses and immune cell trafficking.

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