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Related Experiment Videos

Reactive nitrogen intermediates in human neuropathology: an overview

C F Brosnan1, L Battistini, C S Raine

  • 1Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, N.Y. 10401.

Developmental Neuroscience
|January 1, 1994
PubMed
Summary

In human glial cells, astrocytes produce nitric oxide (NO) in response to cytokines, unlike microglia. This NO production by astrocytes inhibits fungal growth and is observed in multiple sclerosis lesions, differing from rodent responses.

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Area of Science:

  • Neuroimmunology
  • Cellular Biology
  • Biochemistry

Background:

  • Nitric oxide (NO) is a signaling molecule with diverse functions, including vasodilation and antimicrobial activity.
  • Two forms of NO synthase (NOS), constitutive (cNOS) and inducible (iNOS), exist, differing in NO release patterns.
  • In rodents, iNOS is primarily in macrophages and microglia, induced by bacterial products and cytokines, potentially causing CNS toxicity.

Purpose of the Study:

  • To investigate the differential expression and regulation of NO synthase in human glial cells compared to rodents.
  • To determine the role of astrocytes and microglia in NO production in the human central nervous system (CNS).
  • To examine the in vivo relevance of NO production in human inflammatory CNS conditions like multiple sclerosis.

Main Methods:

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  • In vitro studies using cultured human glial cells (astrocytes and microglia) stimulated with cytokines (IL-1, TNF alpha, IFN gamma) and bacterial products.
  • Measurement of NO-like activity and NADPH-diaphorase activity in stimulated glial cells.
  • In vivo analysis of acute multiple sclerosis lesions for NADPH-diaphorase activity and co-localization with inflammatory markers (IL-1, TNF).

Main Results:

  • Human astrocytes, but not microglia, induced NO-like activity upon stimulation with cytokines; bacterial products were ineffective.
  • A combination of IL-1 and TNF alpha or IFN gamma potently stimulated NO production in astrocytes.
  • In human multiple sclerosis lesions, hypertrophic astrocytes exhibited high NADPH-diaphorase activity, co-localizing with IL-1 and TNF, while microglia were nonreactive.

Conclusions:

  • The induction of NO production in human glial cells differs significantly from rodent models.
  • Activated astrocytes are the primary source of NO-like activity in the inflamed human CNS.
  • Astrocyte-derived NO may play a role in host defense, as shown by inhibition of Cryptococcus neoformans growth.