Expression of C5a in the brain does not exacerbate experimental autoimmune encephalomyelitis.

Abstract:

:Complement is implicated in the pathology of neurodegenerative and inflammatory disease in the central nervous system (CNS). Although studies demonstrate that inhibition of complement activation attenuates disease development in the CNS, the specific complement components that contribute to the pathogenesis of CNS diseases remain unclear. To dissect the role of C5a in CNS disease, we developed a transgenic mouse that produces C5a exclusively in the brain using the astrocyte-specific, murine glial fibrillary acidic protein (GFAP) promoter. C5a/GFAP mice develop normally and do not demonstrate any signs of spontaneous inflammation or neurodegeneration with age. Using C5a/GFAP mice, we examined the outcome of the animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). To our surprise the onset and severity of myelin oligodendrocyte glycoprotein-induced EAE was essentially identical between C5a/GFAP and control mice. These results demonstrate that C5a, despite it is pro-inflammatory functions, is not critical to the development and progression of EAE.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Reiman R,Campos Torres A,Martin BK,Ting JP,Campbell IL,Barnum SR

doi

10.1016/j.neulet.2005.08.022

keywords:

subject

Has Abstract

pub_date

2005-12-30 00:00:00

pages

134-8

issue

3

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(05)00918-3

journal_volume

390

pub_type

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