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Bone marrow-derived versus parenchymal sources of inducible nitric oxide synthase in experimental autoimmune encephalomyelitis.

Abstract：

:The role of nitric oxide (NO) in central nervous system (CNS) inflammation is uncertain. Whereas experimental autoimmune encephalomyelitis (EAE) is exacerbated in mice deficient in inducible nitric oxide synthase (iNOS), inhibitor studies have suggested a pro-inflammatory role for NO. These discrepancies may reflect balance between immunoregulatory and neurocytopathologic roles for NO. We investigated selective effects of bone marrow-derived versus CNS parenchymal sources of iNOS in EAE in chimeric mice. Chimeras that selectively expressed or ablated iNOS in leukocytes both showed significant delay in disease onset, with no difference in disease severity. We conclude that bone marrow-derived and CNS parenchymal sources of iNOS-derived NO both play a regulatory role in EAE.

journal_name

J Neuroimmunol

journal_title

Journal of neuroimmunology

authors

Zehntner SP,Bourbonniere L,Hassan-Zahraee M,Tran E,Owens T

doi

10.1016/j.jneuroim.2004.01.020

subject

Has Abstract

pub_date

2004-05-01 00:00:00

pages

70-9

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165572804000438

journal_volume

150

pub_type

杂志文章

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