NDLI: Proteinase-activated receptor 2 is an anti-inflammatory signal for colonic lamina propria lymphocytes in a mouse model of colitis.

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Proteinase-activated receptor 2 is an anti-inflammatory signal for colonic lamina propria lymphocytes in a mouse model of colitis.

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Proteinase-activated receptor 2 is an anti-inflammatory signal for colonic lamina propria lymphocytes in a mouse model of colitis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Palazzetti, B. Wallace, J. L. Fiorucci, S. Mencarelli, A. Hollenberg, M. D. Vergnolle, N. Cirino, G. Distrutti, E. Morelli, A.
Description	Author Affiliation: Fiorucci S ( Clinica di Gastroenterologia ed Endoscopia Digestiva, Dipartimento di Medicina Clinica, Patologia Univesita di Perugia, Perugia 06122, Italy. fiorucci@unipg.it);
Abstract	The proteinase-activated receptor 2 (PAR-2) is a member of a family of G protein-coupled receptors for proteases. Proteases cleave PARs within the extracellular N-terminal domains to expose tethered ligands that bind to and activate the cleaved receptors. PAR-2 is highly expressed in colon in epithelial and neuronal elements. In this study we show that PAR-2 activation prevents the development and induces healing of T helper cell type 1-mediated experimental colitis induced by intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in mice. A role for PAR-2 in the protection against colon inflammation was explored by the use of SLIGRL-NH(2), a synthetic peptide that corresponds to the mouse tethered ligand exposed after PAR-2 cleavage. TNBS-induced colitis was dose-dependently reduced by the administration of SLIGRL-NH(2), whereas the scramble control peptide, LSIGRL-NH(2), was uneffective. This beneficial effect was reflected by increased survival rates, improvement of macroscopic and histologic scores, decrease in mucosal content of T helper cell type 1 cytokines, protein, and mRNA, and a diminished myeloperoxidase activity. SLIGRL-NH(2), but not the scramble peptide, directly inhibited IFN-gamma secretion and CD44 expression on lamina propria T lymphocytes. Protection exerted by PAR-2 in TNBS-treated mice was reverted by injecting mice with a truncated form of calcitonin gene-related peptide and by sensory neurons ablation with the neurotoxin capsaicin. Collectively, these studies show that PAR-2 is an anti-inflammatory receptor in the colon and suggest that PAR-2 ligands might be effective in the treatment of inflammatory bowel diseases.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	24
Volume Number	98
Language	English
Publisher	National Academy of Sciences
Publisher Date	2001-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Colitis Immunology Colon Receptors, Thrombin T-Lymphocytes Animals Antigens, CD44 Biosynthesis Calcitonin Gene-Related Peptide Pharmacology Capsaicin Cells, Cultured Chemically Induced Pathology Prevention & Control Cytology Disease Models, Animal Down-Regulation Enzyme Activation Interferon-gamma Interleukin-12 Interleukin-2 Mice Mice, Inbred BALB C Oligopeptides Peptide Fragments Receptor, PAR-2 Metabolism Drug Effects Trinitrobenzenesulfonic Acid Adverse Effects Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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