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Interleukin 1 beta, tumor necrosis factor-alpha and interleukin 6 decrease nuclear thyroid hormone receptor capacity

M Wolf1, N Hansen, H Greten

  • 1Medizinische Kernklinik und Poliklinik, Universitäts-Krankenhaus Eppendorf, Hamburg, Germany.

European Journal of Endocrinology
|September 1, 1994
PubMed
Summary
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Tumor necrosis factor-alpha, interleukin 1 beta, and interleukin 6 reduce thyroid hormone receptor capacity in liver cells. These cytokines are implicated in non-thyroidal illness during critical illness.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Inflammation Research

Background:

  • Acute inflammatory responses in critical illness involve cytokines like TNF-alpha, IL-1 beta, and IL-6.
  • These cytokines are implicated in the thyroid function changes observed in non-thyroidal illness.

Purpose of the Study:

  • To investigate whether TNF-alpha, IL-1 beta, and IL-6 modify the capacity and/or affinity of nuclear thyroid hormone receptors (TR) in vitro.
  • To study the regulation of TR synthesis in response to these cytokines.

Main Methods:

  • Utilized the human hepatoma cell line Hep-G2.
  • Incubated cells with recombinant cytokines (TNF-alpha, IL-1 beta, IL-6) in serum-free medium.
  • Assessed nuclear TR binding capacity and affinity using [125I]-triiodothyronine in nuclear extracts.

Related Experiment Videos

Main Results:

  • Interleukin 1 beta significantly decreased TR capacity in a dose-dependent manner.
  • Interleukin 6 and TNF-alpha also reduced TR capacity, but only at higher concentrations (≥10 µg/l) and to a lesser extent than IL-1 beta.
  • TR affinity was not significantly altered by any of the tested cytokines.

Conclusions:

  • The study demonstrates that key inflammatory cytokines, particularly IL-1 beta, can downregulate thyroid hormone receptor capacity in liver cells.
  • These findings provide insights into the molecular mechanisms underlying thyroid dysfunction in critical illness and non-thyroidal illness.