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Cytokine-mediated human polymorphonuclear neutrophil phagocytosis: evidence of differential sensitivities to manipulation of intracellular mechanisms.

Authors
  • Garner, C V
  • D'Amico, R
  • Simms, H H
Type
Published Article
Journal
The Journal of surgical research
Publication Date
Jan 01, 1996
Volume
60
Issue
1
Pages
84–90
Identifiers
PMID: 8592438
Source
Medline
License
Unknown

Abstract

Interleukin-1 beta (IL-1 beta) and tumor necrosis factor alpha (TNF-alpha) are well known mediators in infectious processes with pleiotropic effects on a variety of cells. These cytokines are known to upregulate Fc receptor (Fc gamma R)-mediated phagocytosis by human polymorphonuclear neutrophils (PMN) but the mechanisms of this enhanced phagocytosis are not known. We investigated the effects of various alterations in intra- and extracellular events on cytokine-induced phagocytic upregulation. Blockade of mRNA synthesis, protein kinase C activation, or G protein activation prevented enhanced phagocytosis by either cytokine. The PMN phagocytic response to TNF-alpha, but not IL-1 beta, was also blunted by agents interfering with mRNA translation or Fc gamma R recycling.

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