| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 9194533 | Journal of Neuroimmunology | 2005 | 8 Pages |
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.
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Authors
Shingo Kato, Yoshikazu Tsuzuki, Ryota Hokari, Yoshikiyo Okada, Junichi Miyazaki, Koji Matsuzaki, Atsuhiro Iwai, Atsushi Kawaguchi, Shigeaki Nagao, Kazuro Itoh, Hidekazu Suzuki, Toshitaka Nabeshima, Soichiro Miura,