Abstract
Nociceptin/orphanin (Noc/oFQ), endogenous agonist for nociceptin receptor (NOR), is thought to be a stimulator of neurogenic inflammation. We investigated the possible role of Noc/oFQ in the development of colitis using NOR-deficient mice treated with dextran sulfate sodium (DSS). Colitis was significantly improved in NOR-deficient mice against wild-type mice. Expression level of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and infiltrating cells also significantly decreased in NOR-deficient mice against wild-type mice. Nociceptin expression increased in wild-type mice after DSS treatment. These results suggest stimulation by Noc/oFQ deteriorates colonic inflammation via up-regulation of adhesion molecule.
| Original language | English |
|---|---|
| Pages (from-to) | 21-28 |
| Number of pages | 8 |
| Journal | Journal of Neuroimmunology |
| Volume | 161 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - 01-01-2005 |
| Externally published | Yes |
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All Science Journal Classification (ASJC) codes
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology
Cite this
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Role of nociceptin/orphanin FQ (Noc/oFQ) in murine experimental colitis. / Kato, Shingo; Tsuzuki, Yoshikazu; Hokari, Ryota; Okada, Yoshikiyo; Miyazaki, Junichi; Matsuzaki, Koji; Iwai, Atsuhiro; Kawaguchi, Atsushi; Nagao, Shigeaki; Itoh, Kazuro; Suzuki, Hidekazu; Nabeshima, Toshitaka; Miura, Soichiro.
In: Journal of Neuroimmunology, Vol. 161, No. 1-2, 01.01.2005, p. 21-28.Research output: Contribution to journal › Article
TY - JOUR
T1 - Role of nociceptin/orphanin FQ (Noc/oFQ) in murine experimental colitis
AU - Kato, Shingo
AU - Tsuzuki, Yoshikazu
AU - Hokari, Ryota
AU - Okada, Yoshikiyo
AU - Miyazaki, Junichi
AU - Matsuzaki, Koji
AU - Iwai, Atsuhiro
AU - Kawaguchi, Atsushi
AU - Nagao, Shigeaki
AU - Itoh, Kazuro
AU - Suzuki, Hidekazu
AU - Nabeshima, Toshitaka
AU - Miura, Soichiro
PY - 2005/1/1
Y1 - 2005/1/1
N2 - Nociceptin/orphanin (Noc/oFQ), endogenous agonist for nociceptin receptor (NOR), is thought to be a stimulator of neurogenic inflammation. We investigated the possible role of Noc/oFQ in the development of colitis using NOR-deficient mice treated with dextran sulfate sodium (DSS). Colitis was significantly improved in NOR-deficient mice against wild-type mice. Expression level of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and infiltrating cells also significantly decreased in NOR-deficient mice against wild-type mice. Nociceptin expression increased in wild-type mice after DSS treatment. These results suggest stimulation by Noc/oFQ deteriorates colonic inflammation via up-regulation of adhesion molecule.
AB - Nociceptin/orphanin (Noc/oFQ), endogenous agonist for nociceptin receptor (NOR), is thought to be a stimulator of neurogenic inflammation. We investigated the possible role of Noc/oFQ in the development of colitis using NOR-deficient mice treated with dextran sulfate sodium (DSS). Colitis was significantly improved in NOR-deficient mice against wild-type mice. Expression level of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) and infiltrating cells also significantly decreased in NOR-deficient mice against wild-type mice. Nociceptin expression increased in wild-type mice after DSS treatment. These results suggest stimulation by Noc/oFQ deteriorates colonic inflammation via up-regulation of adhesion molecule.
UR - http://www.scopus.com/inward/record.url?scp=20044374866&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=20044374866&partnerID=8YFLogxK
U2 - 10.1016/j.jneuroim.2004.12.006
DO - 10.1016/j.jneuroim.2004.12.006
M3 - Article
VL - 161
SP - 21
EP - 28
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
SN - 0165-5728
IS - 1-2
ER -