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Neutrophils augment the release of TNFalpha from LPS-stimulated macrophages via hydrogen peroxide

D Sredni-Kenigsbuch1, T Kambayashi, G Strassmann

  • 1Interdisciplinary Department, Bar-Ilan University, Ramat Gan, Israel. srednid@mail.biu.ac.il

Immunology Letters
|March 14, 2000
PubMed

Insights

Neutrophils enhance tumor necrosis factor (TNFalpha) release from macrophages stimulated by lipopolysaccharide (LPS). This effect is mediated by hydrogen peroxide and requires neutrophil adherence, suggesting a novel inflammatory pathway.

Area of Science:

  • Immunology
  • Cell Biology

Background:

  • Macrophages play a critical role in immune responses, including the production of pro-inflammatory cytokines like TNFalpha.
  • Neutrophils are key players in acute inflammation and can interact with macrophages.

Purpose of the Study:

  • To investigate the effect of polymorphonuclear cells (neutrophils) on TNFalpha release from macrophages stimulated with LPS.
  • To elucidate the mechanism by which neutrophils influence macrophage TNFalpha production.

Main Methods:

  • Co-culture of human peripheral blood neutrophils with mouse peritoneal macrophages stimulated by LPS.
  • Stimulation of neutrophils with FMLP to assess their effect on TNFalpha release.
  • Use of catalase to investigate the role of hydrogen peroxide.
  • Separation of cells using a porous membrane to assess the necessity of adherence.

Main Results:

  • Neutrophils augmented LPS-induced TNFalpha release from macrophages in a dose-dependent manner.
  • This augmentation was dependent on the presence of neutrophils and was reversed by catalase, indicating the involvement of hydrogen peroxide.
  • Direct addition of hydrogen peroxide to macrophages increased TNFalpha secretion.
  • The effect was abolished when neutrophils and macrophages were separated by a porous membrane, suggesting adherence is necessary.

Conclusions:

  • Hydrogen peroxide released from stimulated neutrophils acts as a mediator to augment TNFalpha release from macrophages.
  • Neutrophil-macrophage interaction, potentially involving adherence and hydrogen peroxide signaling, plays a significant role in modulating inflammatory responses.

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