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J Neuroimmunol. 2000 Jul 10;107(1):21-8.

A catalyst of peroxynitrite decomposition inhibits murine experimental autoimmune encephalomyelitis.

Author information

1
Department of Neurology and Neurosurgery, Washington University School of Medicine, Box 8111, 660 S. Euclid, St. Louis, MO 63110, USA. crossa@neuro.wustl.edu

Abstract

Peroxynitrite (PN), the product of nitric oxide (NO) reacted with superoxide, is generated at sites of inflammation. Nitrotyrosine (NT), a marker of PN formation, is abundant in lesions of acute experimental autoimmune encephalomyelitis (EAE), and in active multiple sclerosis (MS) plaques. To determine whether PN plays a role in EAE pathogenesis, mice induced to develop EAE were treated with a catalyst specific for the decomposition of PN. Because this catalyst has no effect upon NO, using it allowed differentiation of PN-mediated effects from NO-mediated effects. Mice receiving the PN decomposition catalyst displayed less severe clinical disease, and less inflammation and demyelination than control mice. Encephalitogenic T cells could be recovered from catalyst-treated mice, indicating that the PN decomposition catalyst blocked the pathogenic action of PN at the effector stage of EAE, but was not directly toxic to encephalitogenic T cells. PN plays an important role distinct from that of NO in the pathogenesis of EAE, a major model for MS.

PMID:
10808047
DOI:
10.1016/s0165-5728(00)00242-3
[Indexed for MEDLINE]

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