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

Prasanti Guthikonda, Jeffery Baker, David Mattson

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

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
Pages (from-to)133-139
Number of pages7
JournalJournal of Neuroimmunology
Volume82
Issue number2
DOIs
StatePublished - Mar 1998

Fingerprint

Interferon-beta
Astrocytoma
Nitric Oxide
Cell Line
Multiple Sclerosis
Nitric Oxide Synthase Type II
Nitrites
Interleukin-10
Dexamethasone
Cytokines
omega-N-Methylarginine
Therapeutic Uses
Immunosuppressive Agents
Astrocytes
Transforming Growth Factor beta
Pathology
Brain

Keywords

  • 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

Cite this

Interferon-beta-1-b (IFN-B) decreases induced nitric oxide (NO) production by a human astrocytoma cell line. / Guthikonda, Prasanti; Baker, Jeffery; Mattson, David.

In: Journal of Neuroimmunology, Vol. 82, No. 2, 03.1998, p. 133-139.

Research output: Contribution to journalArticle

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