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Development and Identification of a Novel Subpopulation of Human Neutrophil-derived Giant Phagocytes In Vitro
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Triggering receptor expressed on myeloid cells-1 in neutrophil inflammatory responses: differential regulation of

Markus P Radsak1, Helmut R Salih, Hans-Georg Rammensee

  • 1Institute for Cell Biology, Department of Immunology, University of Tübingen, Tuebingen, Germany. markus.radsak@uni-tuebingen.de

Journal of Immunology (Baltimore, Md. : 1950)
|April 7, 2004
PubMed

Insights

Triggering receptor expressed on myeloid cells-1 (TREM-1) activation in neutrophils enhances immune responses like degranulation and phagocytosis. However, TREM-1 signaling counteracts the anti-apoptotic effects of Toll-like receptors, modulating inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Innate Immunity

Background:

  • Polymorphonuclear neutrophils (PMN) are key players in innate host defense against microbial pathogens.
  • The triggering receptor expressed on myeloid cells-1 (TREM-1) is an activating receptor on PMN involved in inflammatory responses.
  • The precise cellular effects of TREM-1 stimulation require further elucidation.

Purpose of the Study:

  • To characterize TREM-1-mediated activation of human PMN at a cellular level.
  • To evaluate the impact of TREM-1 receptor ligation on PMN effector functions.
  • To investigate the interplay between TREM-1 and Toll-like receptor (TLR) signaling in PMN.

Main Methods:

  • Human PMN were stimulated to ligate the TREM-1 receptor.
  • PMN effector functions, including degranulation, respiratory burst, and phagocytosis, were assessed.
  • Synergistic effects of TREM-1 and TLR ligand co-stimulation were evaluated.

Main Results:

  • TREM-1 activation induced immediate degranulation, IL-8 release, respiratory burst, and phagocytosis in PMN.
  • TREM-1 ligation synergized with TLR ligands (LPS, Pam(3)Cys, R-848) in activating PMN.
  • TREM-1 activation neutralized the anti-apoptotic effects of TLR-mediated stimulation on PMN survival.

Conclusions:

  • TREM-1 is a critical mediator of neutrophil inflammatory responses.
  • TREM-1 signaling enhances key PMN effector functions essential for host defense.
  • TREM-1 plays a distinct role in regulating PMN survival, opposing TLR-induced protection from apoptosis.

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