Interferon-beta-1-b (IFN-B) decreases induced nitric oxide (NO) production by a human astrocytoma cell line

Prasanti Guthikonda, Jeffery Baker, David H. Mattson

Research output: Contribution to journalArticle

37 Scopus citations


Inducible nitric oxide synthase (iNOS) is expressed by astrocytes in demyelinating regions of multiple sclerosis (MS) brain plaques, suggesting that NO contributes to MS pathology. Since the immunosuppressive cytokine IFN-B ameliorates MS disease activity, it is of interest to assess the modulatory role of IFN-B on NO production. We studied the effects of IFN-B, as well as dexamethasone, IL-10, and transforming growth factor-beta (TGF- B), on cytokine-induced NO production by the human astrocytoma cell line, A172. L-NMMA and aminoguanidine, competitive inhibitors of iNOS, suppressed NO production as measured by the NO byproduct, nitrite, as did IFN-B. Dexamethasone enhanced NO production, and IFN-B decreased the amount of this enhancement. Neither IL-10 nor TGF-B inhibited nitrite production. The therapeutic effect of IFN-B in MS may be partly due to suppression of pathogenic NO production.

Original languageEnglish (US)
Pages (from-to)133-139
Number of pages7
JournalJournal of Neuroimmunology
Issue number2
StatePublished - Mar 1 1998


  • A172, human astrocytoma cell line
  • Astrocytes
  • Cytokines
  • Dexamethasone
  • Interferon-beta
  • Multiple sclerosis
  • Nitric oxide

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

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