Toll-Interacting Protein Modulates Gut Flora Composition, Epithelial Barrier Integrity and Susceptibility to Colitis
Détails
ID Serval
serval:BIB_8253C695E8CA
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
Toll-Interacting Protein Modulates Gut Flora Composition, Epithelial Barrier Integrity and Susceptibility to Colitis
Titre de la conférence
Annual Meeting of the Swiss Society of Gastroenterology, Swiss Society of Visceral Surgery, Swiss Association of the Study of the Liver and Swiss Society of Clinical Nutrition
Adresse
Interlaken, Switzerland, September 20-21, 2012
ISBN
1424-7860
ISSN-L
0036-7672
Statut éditorial
Publié
Date de publication
2012
Volume
142
Série
Swiss Medical Weekly
Langue
anglais
Résumé
Toll-like receptor ( TLR) s ignals are key to maintaining hostmicrobial
i nteractions. T he T oll-interacting-protein (Tollip) is a
ubiquitously-expressed inhibitor of inflammasome a nd TLR
signaling. W e hypothesized that T ollip might control g ut
homeostasis. G enetic ablation of T ollip d id not lead to
spontaneous colitis b ut h ad d ramatic c onsequences on t he
intestinal expression of the α-defensin cryptidin 4 and the C-type
lectin R EGIIIβ. These c hanges were associated with intestinal
dysbiosis a nd e nhanced colonization b y segmented filamentous
bacteria - a k ey p ro-inflammatory component of the microbiota.
Tollip deficiency increased susceptibility to dextran sulfate sodium
(DSS) colitis and aggravated chronic Th17-driven colitis in IL-10-/-
mice. Flora d epletion w ith a ntibiotics in T ollip-/- mice w as not
sufficient to restore DSS colitis susceptibility and deletion of Tollip
in n on-hematopoietic c ells using bone-marrow chimeras w as
sufficient to increase s usceptibility t o DSS colitis. After D SS
administration, we o bserved several e pithelial defects i n Tollip-/-
mice including early tight junctions disruption, increased epithelial
apoptosis, and increased intestinal permeability. Overall, our data
show that T ollip significantly impacts intestinal h omeostasis by
controlling b acterial ecology and intestinal r esponse to chemical
and immunological stresses.
i nteractions. T he T oll-interacting-protein (Tollip) is a
ubiquitously-expressed inhibitor of inflammasome a nd TLR
signaling. W e hypothesized that T ollip might control g ut
homeostasis. G enetic ablation of T ollip d id not lead to
spontaneous colitis b ut h ad d ramatic c onsequences on t he
intestinal expression of the α-defensin cryptidin 4 and the C-type
lectin R EGIIIβ. These c hanges were associated with intestinal
dysbiosis a nd e nhanced colonization b y segmented filamentous
bacteria - a k ey p ro-inflammatory component of the microbiota.
Tollip deficiency increased susceptibility to dextran sulfate sodium
(DSS) colitis and aggravated chronic Th17-driven colitis in IL-10-/-
mice. Flora d epletion w ith a ntibiotics in T ollip-/- mice w as not
sufficient to restore DSS colitis susceptibility and deletion of Tollip
in n on-hematopoietic c ells using bone-marrow chimeras w as
sufficient to increase s usceptibility t o DSS colitis. After D SS
administration, we o bserved several e pithelial defects i n Tollip-/-
mice including early tight junctions disruption, increased epithelial
apoptosis, and increased intestinal permeability. Overall, our data
show that T ollip significantly impacts intestinal h omeostasis by
controlling b acterial ecology and intestinal r esponse to chemical
and immunological stresses.
Création de la notice
14/02/2013 16:18
Dernière modification de la notice
20/08/2019 15:42
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