J Neuroimmunol 2003 Apr;137(1-2):94-9
Pollak Y, Ovadia H, Orion E, Weidenfeld J, Yirmiya R.
Department of Psychology, The Hebrew University of Jerusalem, Mount Scopus, 91905, Jerusalem, Israel
To elucidate the mechanisms underlying the EAE-associated behavioral syndrome (EBS), we examined the temporal correlation between the behavioral alterations and inflammatory processes.
Onset of the behavioral syndrome was associated with the onset of brain infiltration, as well as mRNA expression of interleukin 1beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha) and elevated production of interleukin 1beta protein and prostaglandin E(2) (PGE(2)).
Sickness behavior symptoms coincided with peak cytokine expression.
Behavioral recovery was associated with a reduction of cytokine expression, but not infiltration, PGE(2) production or motor disturbances.
These results suggest that inflammatory processes in general, and the production of pro-inflammatory cytokines in particular, are involved in mediating EAE-associated sickness behavior.