Substance P receptor mediated maintenance of chronic inflammation in EAE

Emily K. Reinke, Matthew J. Johnson, Changying Ling, Jozsef Karman, Jang Eun Lee, Joel V. Weinstock, Matyas Sandor, Zsuzsa Fabry

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


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 languageEnglish (US)
Pages (from-to)117-125
Number of pages9
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - Nov 2006
Externally publishedYes

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).


  • EAE
  • MS
  • Neurokinin
  • Neuropeptide
  • SR140333
  • Substance P


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