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Interleukin-8 delays spontaneous and tumor necrosis factor-alpha-mediated apoptosis of human neutrophils

R Kettritz1, M L Gaido, H Haller

  • 1Franz-Volhard Clinic, Humboldt University of Berlin, Germany.

Kidney International
|February 7, 1998
PubMed

Insights

Interleukin-8 (IL-8) significantly delays polymorphonuclear neutrophil (PMN) apoptosis, prolonging their lifespan during inflammation. This IL-8 effect on PMN lifespan is independent of Bcl-2 and may involve IL-8 receptors RI and RII.

Area of Science:

  • Immunology
  • Cell Biology
  • Inflammation Research

Background:

  • Polymorphonuclear neutrophils (PMN) are key immune cells involved in inflammation.
  • Cytokines, such as interleukin-8 (IL-8), influence PMN behavior during inflammatory responses.
  • Apoptosis, or programmed cell death, is a critical process regulating PMN lifespan.

Purpose of the Study:

  • To investigate the effect of IL-8 on apoptosis in human PMN.
  • To determine the role of IL-8 receptors (RI and RII) in mediating this effect.
  • To explore the involvement of the Bcl-2 protein in IL-8's influence on PMN apoptosis.

Main Methods:

  • Human PMN were isolated and cultured for up to 30 hours.
  • Apoptosis was assessed using microscopy, DNA fragmentation assays, and flow cytometry.
  • IL-8 receptor involvement and Bcl-2 expression (protein and gene) were analyzed.

Main Results:

  • IL-8 significantly delayed spontaneous PMN apoptosis in a dose-dependent manner.
  • IL-8 also inhibited tumor necrosis factor-alpha (TNF-α)-induced PMN apoptosis.
  • Bcl-2 protein and gene expression were not detected in IL-8-treated PMN, indicating a Bcl-2-independent mechanism.

Conclusions:

  • IL-8 prolongs human neutrophil lifespan in vitro by delaying apoptosis.
  • This anti-apoptotic effect of IL-8 may contribute to a controlled inflammatory response.
  • The IL-8 RII receptor appears to mediate this effect, with potential additional contribution from RI, independent of Bcl-2.

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