Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis
Loading...
Date
2013-04-22
Authors
Kamboj, Amit
Lu, Ping
Cossoy, Michael B
Stobart, Jillian L
Dolhun, Brian A
Kauppinen, Tiina M
de Murcia, Gilbert
Anderson, Christopher M
Journal Title
Journal ISSN
Volume Title
Publisher
Abstract
Abstract
Background
Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis characterized by entry of activated T cells and antigen presenting cells into the central nervous system and subsequent autoimmune destruction of nerve myelin. Previous studies revealed that non-selective inhibition of poly(ADP-ribose) polymerases (PARPs) 1 and 2 protect against neuroinflammation and motor dysfunction associated with EAE, but the role of the PARP-2 isoform has not yet been investigated selectively.
Results
EAE was induced in mice lacking PARP-2, and neurological EAE signs, blood-spine barrier (BSB) permeability, demyelination and inflammatory infiltration were monitored for 35 days after immunization. Mice lacking PARP-2 exhibited significantly reduced overall disease burden and peak neurological dysfunction. PARP-2 deletion also significantly delayed EAE onset and reduced BSB permeability, demyelination and central nervous system (CNS) markers of proinflammatory Th1 and Th17 T helper lymphocytes.
Conclusions
This study represents the first description of a significant role for PARP-2 in neuroinflammation and neurological dysfunction in EAE.
Description
Keywords
Citation
Journal of Neuroinflammation. 2013 Apr 22;10(1):49