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

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.