Tumour necrosis factor alpha stimulates resorption and inhibits synthesis of proteoglycan in cartilage

Nature. 1986 Aug 7-13;322(6079):547-9. doi: 10.1038/322547a0.

Abstract

During inflammatory reactions, activated leukocytes are thought to produce a variety of small proteins (cytokines) that influence the behaviour of other cells (including other leukocytes). Of these substances, which include the interleukins, interferons and tumour necrosis factors (TNFs), interleukin-1 (IL-1) has been considered potentially a most important inflammatory mediator because of its wide range of effects. In vivo it is pyrogenic and promotes the acute phase response; in vitro it activates lymphocytes and stimulates resorption of cartilage and bone. Cartilage resorption is a major feature of inflammatory diseases such as rheumatoid arthritis, and IL-1 is the only cytokine hitherto known to promote it. TNFs are characterized by their effects on tumours and cytotoxicity to transformed cells, but share some actions with IL-1. I report here that recombinant human TNF alpha stimulates resorption and inhibits synthesis of proteoglycan in explants of cartilage. Its action is similar to and additive with IL-1, and it is a second macrophage-derived cytokine whose production in rheumatoid arthritis, or inflammation generally, could contribute to tissue destruction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cartilage / drug effects*
  • Cartilage / metabolism
  • Cattle
  • Chromatography, Gel
  • Culture Techniques
  • Glycoproteins / genetics
  • Glycoproteins / pharmacology*
  • Proteoglycans / metabolism*
  • Recombinant Proteins / pharmacology
  • Swine
  • Time Factors
  • Tumor Necrosis Factor-alpha

Substances

  • Glycoproteins
  • Proteoglycans
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha