Macrophages from Crohn's disease patients exhibit deficient pro-repair functions

Détails

ID Serval
serval:BIB_0D31A8AD8B38
Type
Actes de conférence (partie): contribution originale à la littérature scientifique, publiée à l'occasion de conférences scientifiques, dans un ouvrage de compte-rendu (proceedings), ou dans l'édition spéciale d'un journal reconnu (conference proceedings).
Sous-type
Abstract (résumé de présentation): article court qui reprend les éléments essentiels présentés à l'occasion d'une conférence scientifique dans un poster ou lors d'une intervention orale.
Collection
Publications
Institution
Titre
Macrophages from Crohn's disease patients exhibit deficient pro-repair functions
Titre de la conférence
Annual Meeting of the Swiss Society of Gastroenterology, Swiss Society for Visceral, Surgery Swiss Association for the Study of the Liver, Swiss Association of Clinical Nutrition
Auteur⸱e⸱s
D'Angelo Fabrizia, Bernasconi Eric, Maillard Michel H., Andriamaha Catherine, Bachmann Daniel, Michetti Pierre, Velin Dominique
Adresse
Interlaken, Switzerland, September 23-24, 2010
ISBN
1424-7860
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
140
Série
Swiss Medical Weekly
Pages
4S
Langue
anglais
Notes
Meeting Abstract
Résumé
BACKGROUND: We previously reported that myeloid cells can induce mucosal healing in a mouse model of acute colitis. Promotion of mucosal repair is becoming a major goal in the treatment of Crohn's disease. Our aim in this study is to investigate the pro-repair function of myeloid cells in healthy donor (HD) and Crohn's disease patients (CD).
METHODS: Peripheral blood mononuclear cells (PBMC) from HD and CD patients were isolated from blood samples by Ficoll density gradient. Monocytic CD14+ cells were positively selected by Macs procedure and then differentiated ex-vivo into macrophages (Mφ). The repair function of PBMC, CD14+ monocytic cells and macrophages were evaluated in an in vitro wound healing assay.
RESULTS: PBMC and CD14+ myeloid cells from HD and CD were not able to repair at any tested cell concentration. Remarkably, HD Mφ were able to induce wound healing only at high concentration (105 added Mφ), but, if activated with heat killed bacteria, they were able to repair even at very low concentration. On the contrary, not activated CD Mφ were not able to promote healing at any rate, but this function was restored upon activation.
CONCLUSION: We showed that CD Mφ in their steady state, unlike HD Mφ, are defective in promoting wound healing. Our results are in keeping with the current theory of CD as an innate immunodeficiency. Defective Mφ may be responsible to the mucosal repair defects in CD patients and to the subsequent chronic activation of the adaptive immune response.
Web of science
Création de la notice
04/11/2010 15:44
Dernière modification de la notice
20/08/2019 13:34
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