Resolvin E1 promotes mucosal surface clearance of neutrophils: a new paradigm for inflammatory resolution
Détails
ID Serval
serval:BIB_08912B7DC238
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Resolvin E1 promotes mucosal surface clearance of neutrophils: a new paradigm for inflammatory resolution
Périodique
FASEB Journal
ISSN
1530-6860
Statut éditorial
Publié
Date de publication
10/2007
Peer-reviewed
Oui
Volume
21
Numéro
12
Pages
3162-70
Notes
Journal Article
Research Support, N.I.H., Extramural --- Old month value: Oct
Research Support, N.I.H., Extramural --- Old month value: Oct
Résumé
Migration of neutrophils (PMN) across epithelia is a pathological hallmark of numerous mucosal diseases. Whereas lesions at mucosal surfaces are generally self-limiting, endogenous mechanisms of resolution are incompletely understood. Previous studies revealed that resolvins directly act on PMN to attenuate transendothelial migration, less is known about the influence of resolvins on PMN-epithelial interactions and whether they act on epithelia. We studied the dynamics of resolvin E1 (RvE1) actions on leukocyte transepithelial migration. PMN exposure to RvE1 or chemerin (peptide agonist of ChemR23) reduced transepithelial migration in a concentration-dependent manner. Conversely, activation of epithelial ChemR23 promoted apical clearance of PMN. A nonbiased screen of known PMN ligands expressed on epithelial cells in response to RvE1 revealed selective induction of CD55, an apically expressed antiadhesive molecule. CD55 promoter analysis demonstrated that both RvE1 and chemerin activate the CD55 promoter. Inhibition of CD55 by neutralizing antibody prevented RvE1-dependent augmentation of apical PMN clearance. Taken together these findings implicate a "two-hit" model of inflammatory resolution, whereby activation of the PMN RvE1 receptor attenuates transepithelial migration and subsequent actions on the epithelium promote CD55-dependent clearance of PMN across the epithelial cell surface promoting active inflammatory resolution.
Mots-clé
Animals
Antigens, CD55/genetics/metabolism
Cell Line
Cell Movement/*physiology
Chemokines/metabolism
Eicosapentaenoic Acid/*analogs & derivatives/metabolism
*Epithelial Cells/cytology/immunology/physiology
Humans
Inflammation/*immunology
Intercellular Adhesion Molecule-1/metabolism
Mucous Membrane/cytology/immunology
Neutrophils/cytology/*immunology/physiology
Promoter Regions (Genetics)
Pubmed
Web of science
Création de la notice
18/01/2008 12:11
Dernière modification de la notice
20/08/2019 12:30