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, ) pendant 10 min, suivie de streptavidine-peroxydase (Kit Abcam Kit IHC de détection de HRP/DAB (ABC) spécifique de lapin (réf: ab64261 Abcam, Cambridge, Royaume-Uni) pendant 10 min. Les sections ont ensuite été incubées avec AEC (Leica Biosystems Ltd, Apre?s de?paraffinisation des coupes (4 µM d'e?paisseur), elles ont e?te?pre?traite?ese?te?pre?traite?es dans un tampon citrate, vol.1, p.400
, Notre hypothèse de base est que le régime MDD, le régime HE, les LPS du microbiote et l'inflammation intestinale (modèle Dextran Sodium Sulfate (DSS) comme déclencheurs et l'immunité innée en tant que modulateur font partie d'un même sce?nario conduisant à la NASH. Des rats carencés (MDD), soumis ou non au régime riche en graisse à l'âge adulte (HE) et expose?s ou non à deux inducteurs de l'inflammation locale et syste?mique, le DSS (inflammation intestinale) et les LPS (effets syste?miques de l'inflammation intestinale) ont été étudiés. Nous n'observons pas d'alte?ration de l'immuniteínne?e (TLR4) dans les groupes MDD/DSS, MDD/HE et MDD/HE/LPS. L'inflammation observe?e au niveau intestinal chez les rats MDD/DSS est également observée au niveau hépatique, avec de stéatose et activation de l'inflammasome et de la chimiokine MCP-1 et IL-1beta. De façon surprenante, cet effet systémique ne met pas en jeu la voie TLR4 et son ligand LPS même quand les rats étaitent exposés au LPS, pendant la gestation et la lactation produit une stéato-hépatite non alcoolique (NASH) chez les animaux soumis au re?gime riche en graisses (HE) pendant l'âge adulte, en de?pit d'une normalisation histologique et métabolique par un régime normal entre le sevrage (J21) et l'âge de puberté (J50)
mais pas par l'activation de TLR4 par translocation de LPS. L'immuniteínne?e n' étant pas impliquée même par l'injection directe du LPS, les effets respectifs et synergiques de régime MDD ,
, Our basic assumption is that MDD, HE diet, microbiota LPS and intestinal inflammation (Dextran Sodium Sulfate (DSS) model) as triggers and innate immunity as a modulator are part of the same scenario leading to NASH. Deficient rats (MDD), whether or not exposed to the high-fat diet in adulthood (HE) and whether or not exposed to two inducers of local and systemic inflammation, DSS (intestinal inflammation) or LPS (systemic effects intestinal inflammation) were studied. We did not observe alterations in innate immunity (TLR4) in the MDD/DSS, MDD/HE and MDD/HE/LPS groups. Inflammation observed in the intestines in MDD/DSS rats is also observed in the liver, with steatosis and activation of the inflammasome and chemokine MCP-1 and IL-1beta. Surprisingly, this systemic effect does not involve the TLR4 pathway and its ligand LPS even when the rats were exposed to LPS directly at the peritoneal level. Our study conclude that NASH favored by the systemic effects of Intestinal inflammation is mediated by MCP-1/IL-1?, but not by activation of TLR4 by translocation of LPS, Mots clés: Foie, maladie intestinale inflammatoire, récepteur Toll-like 4, Lipopolysaccarides, inflammation. Summary: Deficiency of methyl donors (folic acid and vitamin B12) (MDD) during pregnancy and lactation produces non-alcoholic steatohepatitis (NASH) in animals fed high fat (HE) diet, despite histological and metabolic normalization by a normal diet between weaning (J21) and puberty (J50)