Local Treatment with Lactate Prevents ...
Type de document :
Compte-rendu et recension critique d'ouvrage
DOI :
PMID :
Titre :
Local Treatment with Lactate Prevents Intestinal Inflammation in the TNBS-Induced Colitis Model.
Auteur(s) :
Iraporda, Carolina [Auteur]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Romanin, David E [Auteur]
Instituto de Estudios Inmunológicos y Fisiopatológicos [Buenos Aires, Argentina] [IIPF]
Bengoa, Ana A [Auteur]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Errea, Agustina J [Auteur]
Instituto de Estudios Inmunológicos y Fisiopatológicos [Buenos Aires, Argentina] [IIPF]
Cayet, delphine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Foligné, Benoit [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Sirard, Jean-Claude [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Garrote, Graciela L [Auteur]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Abraham, Analía G [Auteur]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Área bioquímica y control de alimentos [La Plata]
Rumbo, Martín [Auteur correspondant]
Instituto de Estudios Inmunológicos y Fisiopatológicos [Buenos Aires, Argentina] [IIPF]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Romanin, David E [Auteur]
Instituto de Estudios Inmunológicos y Fisiopatológicos [Buenos Aires, Argentina] [IIPF]
Bengoa, Ana A [Auteur]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Errea, Agustina J [Auteur]
Instituto de Estudios Inmunológicos y Fisiopatológicos [Buenos Aires, Argentina] [IIPF]
Cayet, delphine [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Foligné, Benoit [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Sirard, Jean-Claude [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Garrote, Graciela L [Auteur]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Abraham, Analía G [Auteur]
Centro de Investigación y Desarrollo en Criotecnología de Alimentos [CIDCA]
Área bioquímica y control de alimentos [La Plata]
Rumbo, Martín [Auteur correspondant]
Instituto de Estudios Inmunológicos y Fisiopatológicos [Buenos Aires, Argentina] [IIPF]
Titre de la revue :
Frontiers in Immunology
Pagination :
651
Éditeur :
Frontiers
Date de publication :
2016-12-27
ISSN :
1664-3224
Mot(s)-clé(s) en anglais :
lactate
innate immunity
flagellin
immunomodulation
TnBs-induced colitis
innate immunity
flagellin
immunomodulation
TnBs-induced colitis
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Lactate has long been considered as a metabolic by-product of cells. Recently, this view has been changed by the observation that lactate can act as a signaling molecule and regulates critical functions of the immune system. ...
Lire la suite >Lactate has long been considered as a metabolic by-product of cells. Recently, this view has been changed by the observation that lactate can act as a signaling molecule and regulates critical functions of the immune system. We previously identified lactate as the component responsible for the modulation of innate immune epithelial response of fermented milk supernatants in vitro. We have also shown that lactate downregulates proinflammatory responses of macrophages and dendritic cells. So far, in vivo effects of lactate on intestinal inflammation have not been reported. We evaluated the effect of intrarectal administration of lactate in a murine model of colitis induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). The increase in lactate concentration in colon promoted protective effects against TNBS-induced colitis preventing histopathological damage, as well as bacterial translocation and rise of IL-6 levels in serum. Using intestinal epithelial reporter cells, we found that flagellin treatment induced reporter gene expression, which was abrogated by lactate treatment as well as by glycolysis inhibitors. Furthermore, lactate treatment modulated glucose uptake, indicating that high levels of extracellular lactate can impair metabolic reprograming induced by proinflammatory activation. These results suggest that lactate could be a potential beneficial microbiota metabolite and may constitute an overlooked effector with modulatory properties.Lire moins >
Lire la suite >Lactate has long been considered as a metabolic by-product of cells. Recently, this view has been changed by the observation that lactate can act as a signaling molecule and regulates critical functions of the immune system. We previously identified lactate as the component responsible for the modulation of innate immune epithelial response of fermented milk supernatants in vitro. We have also shown that lactate downregulates proinflammatory responses of macrophages and dendritic cells. So far, in vivo effects of lactate on intestinal inflammation have not been reported. We evaluated the effect of intrarectal administration of lactate in a murine model of colitis induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). The increase in lactate concentration in colon promoted protective effects against TNBS-induced colitis preventing histopathological damage, as well as bacterial translocation and rise of IL-6 levels in serum. Using intestinal epithelial reporter cells, we found that flagellin treatment induced reporter gene expression, which was abrogated by lactate treatment as well as by glycolysis inhibitors. Furthermore, lactate treatment modulated glucose uptake, indicating that high levels of extracellular lactate can impair metabolic reprograming induced by proinflammatory activation. These results suggest that lactate could be a potential beneficial microbiota metabolite and may constitute an overlooked effector with modulatory properties.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
Source :
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- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5187354/pdf
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