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Impact of interleukin-17 on macrophage phagocytosis of apoptotic neutrophils and particles.

Authors
  • Silverpil, Elin
  • Glader, Pernilla
  • Hansson, Marit
  • Lindén, Anders
Type
Published Article
Journal
Inflammation
Publisher
Springer-Verlag
Publication Date
Feb 01, 2011
Volume
34
Issue
1
Pages
1–9
Identifiers
DOI: 10.1007/s10753-010-9201-8
PMID: 20339909
Source
Medline
License
Unknown

Abstract

There is now substantial evidence that the cytokine interleukin-17 orchestrates the accumulation of neutrophils in mammals and thereby contributes to host defense. However, the role of IL-17 in controlling neutrophil turnover is not fully understood. Here, we demonstrate that IL-17 stimulates the apoptosis of mouse neutrophils and, simultaneously, the release of the microbicidal compound, myeloperoxidase. IL-17 also stimulates mouse macrophages to phagocytose aged neutrophils and latex beads, and it induces an increase in a soluble form of the phagocytic receptor, lectin-like oxidized low-density lipoprotein receptor-1 as well. In contrast, IL-17 does not markedly increase the release of the archetype neutrophil-recruiting cytokine, macrophage inflammatory protein-2 in mouse macrophages. Importantly, IL-17 also stimulates the phagocytosis of latex beads in human monocyte-derived macrophages. Thus, IL-17 bears the potential to control both phagocytosis and neutrophil turnover during activation of host defense.

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