IL-1 beta and TNF alpha, but not IL-6, induce alpha 1-antichymotrypsin expression in the human astrocytoma cell line U373 MG

Neuroreport. 1995 Nov 27;6(17):2283-6. doi: 10.1097/00001756-199511270-00004.

Abstract

Cytokines such as interleukin-1 (IL-1) and interleukin-6 (IL-6) have previously been shown to participate in neurodegenerative processes including Alzheimer's disease. However, the molecular consequences of increased cytokine expression in the brain remain largely unknown. We have studied the effects of IL-1, IL-6 and TNF alpha on the expression of the acute-phase protein alpha 1-antichymotrypsin (ACT) in human astrocytoma cell lines. Both IL-1 and TNF alpha, but not IL-6, were able to induce ACT gene transcription and protein synthesis. The synthetic glucocorticoid dexamethasone enhanced cytokine-induced ACT mRNA expression and protein synthesis. We conclude that IL-1-induced expression of ACT may be part of the inflammatory response in the brain and may be involved in the pathology of Alzheimer's disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents / pharmacology
  • Astrocytoma / metabolism*
  • Blotting, Northern
  • Dexamethasone / pharmacology
  • Humans
  • Interleukin-1 / pharmacology*
  • Interleukin-6 / pharmacology*
  • Precipitin Tests
  • RNA, Messenger / biosynthesis
  • Serine Proteinase Inhibitors / biosynthesis*
  • Stimulation, Chemical
  • Transcription, Genetic
  • Tumor Cells, Cultured
  • Tumor Necrosis Factor-alpha / pharmacology*
  • alpha 1-Antichymotrypsin / biosynthesis*

Substances

  • Anti-Inflammatory Agents
  • Interleukin-1
  • Interleukin-6
  • RNA, Messenger
  • Serine Proteinase Inhibitors
  • Tumor Necrosis Factor-alpha
  • alpha 1-Antichymotrypsin
  • Dexamethasone