Critical role of P-selectin-dependent leukocyte recruitment in endotoxin-induced intestinal barrier dysfunction in mice.

Détails

ID Serval
serval:BIB_373DE37662B8
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Critical role of P-selectin-dependent leukocyte recruitment in endotoxin-induced intestinal barrier dysfunction in mice.
Périodique
Inflammation Research
Auteur(s)
Mangell P., Mihaescu A., Wang Y., Schramm R., Jeppsson B., Thorlacius H.
ISSN
1023-3830
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
56
Numéro
5
Pages
189-194
Langue
anglais
Résumé
OBJECTIVE: To define the importance of leukocyte recruitment in endotoxin-induced gut permeability. MATERIALS AND METHODS: 31 male C57BL/6 mice were challenged with lipopolysaccharide (LPS). Ileal permeability was measured in Ussing chambers and leukocyte-endothelium interactions studied with intravital fluorescence microscopy after 18 h. RESULTS: LPS caused a clear-cut increase in leukocyte accumulation and intestinal permeability. Immunoneutralisation of P-selectin not only reduced leukocyte recruitment significantly (54 % reduction) but also abolished endotoxin-induced intestinal leakage. Intestinal levels of pro-inflammatory chemokines increased markedly in response to LPS but were not influenced by inhibition of P-selectin in vivo. CONCLUSION: The present study shows not only that endotoxin-induced leukocyte recruitment is mediated by P-selectin but also that sepsis-associated intestinal leakage in the gut is largely regulated by leukocyte accumulation. Thus, our novel data demonstrate a critical link between P-selectin-dependent leukocyte recruitment and gut barrier failure in endotoxemia.
Mots-clé
Animals, Cell Membrane Permeability, Cell Movement, Chemokine CXCL2, Chemokines, Endotoxemia, Endotoxins, Ileum, Interleukin-8, Intestinal Absorption, Leukocytes, Male, Mice, Mice, Inbred C57BL, P-Selectin
Pubmed
Web of science
Création de la notice
13/05/2009 10:48
Dernière modification de la notice
03/03/2018 16:04
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