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

doi:10.1016/j.jneuroim.2006.07.010

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 journal › Article › peer-review

31 Scopus citations

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	https://doi.org/10.1016/j.jneuroim.2006.07.010
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

Publisher link

10.1016/j.jneuroim.2006.07.010

Find It

Find It at U of M Libraries

Cite this

@article{771cd21baa9c4638a458f5d8c0110e8e,

title = "Substance P receptor mediated maintenance of chronic inflammation in EAE",

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.",

keywords = "EAE, MS, Neurokinin, Neuropeptide, SR140333, Substance P",

author = "Reinke, {Emily K.} and Johnson, {Matthew J.} and Changying Ling and Jozsef Karman and Lee, {Jang Eun} and Weinstock, {Joel V.} and Matyas Sandor and Zsuzsa Fabry",

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).",

year = "2006",

month = nov,

doi = "10.1016/j.jneuroim.2006.07.010",

language = "English (US)",

volume = "180",

pages = "117--125",

journal = "Advances in Neuroimmunology",

issn = "0165-5728",

publisher = "Elsevier",

number = "1-2",

}

TY - JOUR

T1 - Substance P receptor mediated maintenance of chronic inflammation in EAE

AU - Reinke, Emily K.

AU - Johnson, Matthew J.

AU - Ling, Changying

AU - Karman, Jozsef

AU - Lee, Jang Eun

AU - Weinstock, Joel V.

AU - Sandor, Matyas

AU - Fabry, Zsuzsa

N1 - 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).

PY - 2006/11

Y1 - 2006/11

N2 - 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.

AB - 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.

KW - EAE

KW - MS

KW - Neurokinin

KW - Neuropeptide

KW - SR140333

KW - Substance P

UR - http://www.scopus.com/inward/record.url?scp=33750610585&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750610585&partnerID=8YFLogxK

U2 - 10.1016/j.jneuroim.2006.07.010

DO - 10.1016/j.jneuroim.2006.07.010

M3 - Article

C2 - 16942803

AN - SCOPUS:33750610585

VL - 180

SP - 117

EP - 125

JO - Advances in Neuroimmunology

JF - Advances in Neuroimmunology

SN - 0165-5728

IS - 1-2

ER -

Substance P receptor mediated maintenance of chronic inflammation in EAE

Abstract

Bibliographical note

Keywords

Publisher link

Find It

Other files and links

Fingerprint

Cite this