Abstract
Substance P (SP) is a modulatory, pro-inflammatory neuropeptide. We investigated the role of the SP receptor, neurokinin-1 (NK-1), in EAE. Our data show that in the chronic phase, mice lacking NK-1 have improved mobility and decreased numbers of LFA-1 high CD4+ T cells and MOG-specific, IFN-γ producing CD4+ T cells. SR140333, an NK-1 antagonist, administered alone during the chronic phase of EAE was not sufficient to ameliorate symptoms. These results indicate that SP, through NK-1, contributes to maintenance of CNS inflammation, and combining NK-1 antagonists with conventional anti-inflammatory treatments may enhance the success of treatments for diseases like multiple sclerosis.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 117-125 |
| Number of pages | 9 |
| Journal | Journal of Neuroimmunology |
| Volume | 180 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Nov 2006 |
| Externally published | Yes |
Bibliographical note
Funding Information:We thank Toshi Kinoshita of the histopathology service of the University of Wisconsin Medical School Department of Pathology and Laboratory Medicine for expert histology services, other members of the laboratory for assistance with flow cytometry and other experiments, Bo Huang of the University of Wisconsin-Madison Statistics Department for statistical consulting, Dr. Laura Hogan for critical reading of the manuscript. This work was supported by the National Institutes of Health (grant RO1-NS 37570 01A2 to Z. Fabry).
Keywords
- EAE
- MS
- Neurokinin
- Neuropeptide
- SR140333
- Substance P
