Abstract
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 1β (IL-1β) and tumor necrosis factor α (TNF-α) and elevated production of interleukin 1β protein and prostaglandin E2 (PGE2). Sickness behavior symptoms coincided with peak cytokine expression. Behavioral recovery was associated with a reduction of cytokine expression, but not infiltration, PGE2 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.
| Original language | English |
|---|---|
| Pages (from-to) | 94-99 |
| Number of pages | 6 |
| Journal | Journal of Neuroimmunology |
| Volume | 137 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Apr 2003 |
Bibliographical note
Funding Information:The authors thank Orli Bar-Shalev, Shira Gur, Lior Friedman, Yael Perets, Meital Shahar, Michal Shlayer, Michal Shuker and Gili Wolf for their excellent help in running the experiments. The research was supported by a grant from the Israel Science Foundation (No. 820/00) and in part by the Lena P. Harvey Endowment Fund for Neurological Research. RY is a member of the Eric Roland Center for Neurodegenerative Diseases at the Hebrew University of Jerusalem.
Keywords
- EAE
- Infiltration
- Interleukin 1β (IL-1β)
- Prostaglandin E
- Sickness behavior
- TNF-α