Location of Repository

Journal of Leukocyte Biology 47:21 7-223 (1990) Activation of Neutrophils by Cachectin/Tumor Necrosis Factor: Priming of N-Formyl-Methionyl-Leucyl- Phenylalanine-Induced Oxidative Responsiveness Via Receptor Mobilization Without Degranulation

By Steven D. Tennenberg and Joseph S. Solomkin


Human recombinant cachectin/tumor necrosis factor (TNF) was shown to prime neutrophils (PMN8), in a dose-dependent fashion, for subsequent oxidative responsiveness toward n-formyl-methionyl-leucyl-phenylalanine (FMLP). One basis for this phenomenon appeared to be TNF-mediated FMLP receptor mobilization. The maximal observed priming response was associated with a nearly twofold increase in the expression of PMN FMLP surface receptors, without changes in receptor affinity. Priming was not seen following stimulation with phorbol myristate acetate, possibly eliminating a role for the protein kinase C-dependent transductional components of FMLP-induced oxidative activity In the priming process. FMLP receptor mobilization occurred without significant degranulation as evident by an absence of increased granular enzyme release. These data support a potential role of macrophage-derived TNF in the augmentation of PMN host-defense during infectious and inflammatory challenge. TNF-mediated PMN oxidative priming may also promote oxidant tissue injury as seen in septic shock, adult respiratory distress syndrome, and multiple system organ failure. Key words: phorbol myristate acetate, superoxide, inflammatio

Year: 2013
OAI identifier: oai:CiteSeerX.psu:
Provided by: CiteSeerX
Download PDF:
Sorry, we are unable to provide the full text but you may find it at the following location(s):
  • http://citeseerx.ist.psu.edu/v... (external link)
  • http://www.jleukbio.org/conten... (external link)
  • Suggested articles

    To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.