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Macrophage-neutrophil interaction: a paradigm for chronic inflammation revisited

D L Lefkowitz1, S S Lefkowitz

  • 1Department of Microbiology and Immunology, College of Medicine, University of South Florida, Tampa, Florida 33612-4799, USA. slefkowi@tampabay.rr.com

Immunology and Cell Biology
|September 21, 2001
PubMed

Insights

Inactive myeloperoxidase (iMPO) binds to macrophage receptors, inducing pro-inflammatory cytokines like TNF. This highlights iMPO

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Macrophages are known producers of pro-inflammatory cytokines.
  • Previous research indicated that inactive myeloperoxidase (iMPO) binding to macrophage-mannose receptors induces TNF and other cytokines.
  • Endothelial cells also show cytokine mRNA and cytokine upregulation when incubated with iMPO, but not active MPO.

Purpose of the Study:

  • To investigate the dichotomous functions of myeloperoxidase (MPO).
  • To elucidate the role of iMPO as an immunoregulatory molecule.
  • To understand the interaction between neutrophils, endothelial cells, and macrophages in inflammation.

Main Methods:

  • Incubation of endothelial cells with iMPO and enzymatically active MPO.
  • Analysis of cytokine mRNA and cytokine expression.
  • Investigation of iMPO binding to macrophage-mannose receptors.

Main Results:

  • Inactive myeloperoxidase (iMPO) induces TNF and other cytokines via macrophage-mannose receptor binding.
  • iMPO, not active MPO, upregulates cytokine mRNA and cytokines in endothelial cells.
  • Data suggest a functional dichotomy: active MPO for cell killing, iMPO for immune regulation.

Conclusions:

  • Myeloperoxidase exhibits distinct functions: active MPO in cytotoxicity and iMPO in immune regulation.
  • iMPO acts as an immunoregulatory molecule, inducing cytokines and perpetuating inflammation.
  • This interaction among neutrophils, endothelial cells, and macrophages is crucial in TNF induction and inflammation, potentially relevant in diseases like rheumatoid arthritis.

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