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Microglial cell cytotoxicity of oligodendrocytes is mediated through nitric oxide.

J E Merrill, L J Ignarro, M P Sherman, J Melinek and T E Lane
J Immunol August 15, 1993, 151 (4) 2132-2141;
J E Merrill
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L J Ignarro
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M P Sherman
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J Melinek
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T E Lane
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Abstract

Rat ameboid microglia are able to lyse rat oligodendrocytes in vitro. The lysis is inhibited by transforming growth factor-beta, antagonists of nitric oxide (NO) production, as well as antibodies to TNF-alpha, intercellular adhesion molecule-1 (ICAM-1), and leukocyte functional Ag-1. Ameboid microglial cells spontaneously produce detectable levels of the NO metabolite nitrite (NO2-). Stimuli such as PMA, LPS, and/or IFN-gamma induce micromolar concentrations of NO2- within 24 h. TNF-alpha increases IFN gamma but not LPS-induced NO2- production. Incubation with target oligodendrocytes also increases NO2- production in a contact-dependent manner. NO2- production is inhibited by NO synthase antagonists, transforming growth factor-beta, and anti TNF-alpha. Neither antileukocyte functional Ag-1 nor anti-ICAM-1 inhibit NO2- production by microglia in the presence or absence of oligodendrocytes. Indeed, anti-ICAM-1 treatment increases NO2- production. There is a correlation between ameboid microglial cell killing of oligodendrocytes and NO2- production suggesting NO may be a mechanism of death of the oligodendrocyte and possibly play a role in lesion formation in multiple sclerosis.

  • Copyright © 1993 by American Association of Immunologists

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The Journal of Immunology
Vol. 151, Issue 4
15 Aug 1993
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Microglial cell cytotoxicity of oligodendrocytes is mediated through nitric oxide.
J E Merrill, L J Ignarro, M P Sherman, J Melinek, T E Lane
The Journal of Immunology August 15, 1993, 151 (4) 2132-2141;

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Microglial cell cytotoxicity of oligodendrocytes is mediated through nitric oxide.
J E Merrill, L J Ignarro, M P Sherman, J Melinek, T E Lane
The Journal of Immunology August 15, 1993, 151 (4) 2132-2141;
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Print ISSN 0022-1767        Online ISSN 1550-6606