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Isolation and Characterization of Neutrophils with Anti-Tumor Properties
10:15

Isolation and Characterization of Neutrophils with Anti-Tumor Properties

Published on: June 19, 2015

Polymorphonuclear granulocytes enhance lipopolysaccharide-induced soluble p75 tumor necrosis factor receptor release

E Lien1, N B Liabakk, A C Johnsen

  • 1Institute of Cancer Research and Molecular Biology, University of Trondheim, University Medical Centre, Norway.

European Journal of Immunology
|September 1, 1995
PubMed

Insights

Lipopolysaccharide (LPS) stimulates the release of soluble tumor necrosis factor receptors (sTNFR). Mononuclear cells and endothelial cells are identified as key sources of specific sTNFR types during Gram-negative infections.

Area of Science:

  • Immunology
  • Cell Biology
  • Microbiology

Background:

  • Lipopolysaccharide (LPS) from Gram-negative bacteria triggers tumor necrosis factor (TNF) release.
  • Soluble TNF receptors (sTNFR), specifically p55 and p75, can neutralize harmful TNF effects during infections.
  • Understanding sTNFR release dynamics is crucial for managing Gram-negative infections like meningococcal septic shock.

Purpose of the Study:

  • To investigate the impact of LPS on the release of soluble TNF receptors (sTNFR) p55 and p75.
  • To identify specific human cell types responsible for sTNFR release upon LPS stimulation.
  • To compare the potency of different LPS types in inducing sTNFR release.

Main Methods:

  • Whole human blood and isolated blood cell populations (mononuclear cells, polymorphonuclear granulocytes) were stimulated with LPS.
  • Co-culture experiments were performed to assess cell interactions.
  • Adherent monocytes and human umbilical vein endothelial cells were stimulated with LPS, and sTNFR release was measured.
  • Flow cytometry was used to analyze TNFR distribution on monocyte membranes.
  • Different LPS types (Neisseria meningitidis and Escherichia coli) were used for comparative analysis.

Main Results:

  • LPS selectively increased soluble p75 TNFR levels in whole blood, with no change in p55 TNFR.
  • Mononuclear cells (PBMC) were the primary source of LPS-induced p75 TNFR release.
  • Co-culturing PBMC with granulocytes enhanced LPS-induced p75 TNFR release.
  • Adherent monocytes selectively released p75 TNFR, with Neisseria meningitidis LPS being significantly more potent than E. coli LPS.
  • LPS stimulation increased the membrane distribution of both TNFR on monocytes.
  • Human umbilical vein endothelial cells selectively released p55 TNFR upon LPS stimulation.

Conclusions:

  • Mononuclear cells are likely a major source of soluble p75 TNFR in Gram-negative sepsis.
  • Endothelial cells may be the primary source of soluble p55 TNFR during Gram-negative sepsis.
  • The in vitro release kinetics of sTNFR may differ from in vivo dynamics.

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