Poly(ADP-ribose) polymerase 2 contributes to neuroinflammation and neurological dysfunction in mouse experimental autoimmune encephalomyelitis

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. © 2013 kamboj et al.; licensee biomed central ltd.