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Inhibitory effects of nicotinamide on intercellular adhesion molecule-1 expression on cultured human thyroid cells

Y Hiromatsu1, M Sato, K Tanaka

  • 1Department of Medicine, Kurume University School of Medicine, Fukuoka, Japan.

Immunology
|October 1, 1993
PubMed

Insights

Nicotinamide and 3-aminobenzamide inhibit intercellular adhesion molecule-1 (ICAM-1) expression on thyroid cells in Graves' disease. This suppression mechanism does not involve free radical scavenging, suggesting potential therapeutic pathways.

Area of Science:

  • Endocrinology
  • Immunology
  • Molecular Biology

Background:

  • Graves' disease involves autoimmune thyroiditis, characterized by elevated intercellular adhesion molecule-1 (ICAM-1) on thyroid cells.
  • ICAM-1 plays a crucial role in immune cell adhesion and infiltration into the thyroid gland.
  • Inhibitors of poly (ADP ribose) synthetase, such as nicotinamide and 3-aminobenzamide (3-AB), are being explored for their potential immunomodulatory effects.

Purpose of the Study:

  • To investigate the effects of nicotinamide and 3-AB on phytohaemagglutinin (PHA)- or interferon-gamma (IFN-gamma)-induced ICAM-1 expression in cultured thyroid cells from Graves' disease patients.
  • To determine if the inhibitory mechanism involves free radical scavenging.

Main Methods:

  • Primary cultured thyroid cells from Graves' disease patients were treated with IFN-gamma or PHA in the presence of nicotinamide, 3-AB, superoxide dismutase, or catalase.
  • Surface expression of ICAM-1 was quantified using flow cytometry.

Main Results:

  • Nicotinamide and 3-AB demonstrated a dose-dependent inhibition of ICAM-1 induction by both IFN-gamma and PHA.
  • Free-radical scavengers, catalase and superoxide dismutase, did not inhibit ICAM-1 expression.
  • These findings suggest that the suppression of ICAM-1 by nicotinamide is not mediated by free radical scavenging.

Conclusions:

  • Nicotinamide and 3-AB effectively suppress ICAM-1 expression on thyroid cells in a Graves' disease model.
  • The mechanism of suppression is independent of free radical scavenging.
  • Further research is warranted to explore the potential of these inhibitors in modulating autoimmune responses within the thyroid gland.

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