Protection against a lethal dose of endotoxin by an inhibitor of tumour necrosis factor processing

Nature. 1994 Jul 21;370(6486):218-20. doi: 10.1038/370218a0.

Abstract

Tumour necrosis factor (tumour necrosis factor-alpha/cachectin) plays a critical role in certain physiological defensive responses but causes severe damage to the host organism when produced in excess. There are two forms of tumour necrosis factor, a type II membrane protein of relative molecular mass 26,000 (26K) and a soluble, 17K form generated from the cell-bound protein by proteolytic cleavage. The two forms of tumour necrosis factor and lymphotoxin-alpha (tumour necrosis factor-beta/lymphotoxin), a related protein, have similar but apparently not identical biological activities. A therapeutic agent which inhibited the release of tumour necrosis factor, but did not reduce the cell-associated activity or the level of lymphotoxin-alpha, might preserve the benefits of these cytokines while preventing tumour necrosis factor-induced damage. Here we describe a potent inhibitor of tumour necrosis factor processing and report that it protects mice from a lethal dose of endotoxin.

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Cell Line
  • Humans
  • Hydroxamic Acids / pharmacology
  • Lymphotoxin-alpha / metabolism
  • Metalloendopeptidases / antagonists & inhibitors
  • Mice
  • Mice, Inbred BALB C
  • Molecular Sequence Data
  • Protein Processing, Post-Translational / drug effects*
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / toxicity

Substances

  • Hydroxamic Acids
  • Lymphotoxin-alpha
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha
  • Metalloendopeptidases