Augmentative effects of tumor necrosis factor-alpha (human, natural type) on polymorphonuclear leukocyte-derived superoxide generation induced by various stimulants

Int J Immunopharmacol. 1992 Nov;14(8):1391-8. doi: 10.1016/0192-0561(92)90010-i.

Abstract

We investigated the effects of tumor necrosis factor-alpha (human, natural type: n-TNF) on polymorphonuclear leukocyte (PMN)-derived superoxide generation by the new method of Cypridina luciferin analog-dependent chemiluminescence, which had high sensitivity and specificity to superoxide. Preincubation of PMNs with n-TNF for 3 min increased PMN-derived superoxide generation induced by phorbol myristate acetate, A23187, opsonized zymosan and N-formyl-methionyl-leucyl-phenylalanine in a concentration dependent manner (0.5-50 Japan reference units/ml of n-TNF). In addition, the enhanced PMN-derived superoxide generation by n-TNF showed a positive correlation to the preincubation time of PMNs with n-TNF (3-15 min). However, a direct incubation of PMNs with n-TNF for 1 h did not induce superoxide from PMNs without the above stimulants. The augmentative effects of n-TNF on PMN-derived superoxide generation should be useful in the PMN-mediated host defense mechanism, such as bactericidal and antitumor activity. The local concentration of n-TNF and the n-TNF-PMN contact time are considered very important in obtaining these effects more efficiently in addition to the presence of PMN-stimulants including complements, chemotactic peptides and phorbol esters.

MeSH terms

  • Dose-Response Relationship, Drug
  • Drug Synergism
  • Humans
  • N-Formylmethionine Leucyl-Phenylalanine / pharmacology
  • NADH, NADPH Oxidoreductases / physiology
  • NADPH Oxidases
  • Neutrophils / drug effects*
  • Neutrophils / metabolism
  • Protein Kinase C / physiology
  • Superoxides / metabolism*
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • Tumor Necrosis Factor-alpha
  • Superoxides
  • N-Formylmethionine Leucyl-Phenylalanine
  • NADH, NADPH Oxidoreductases
  • NADPH Oxidases
  • Protein Kinase C