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Tian, X.* ; Li, R.* ; Jiang, Y. ; Zhao, F.* ; Yu, Z.* ; Wang, Y.* ; Dong, Z.* ; Liu, P.* ; Li, X.*

Bifidobacterium breve ATCC15700 pretreatment prevents alcoholic liver disease through modulating gut microbiota in mice exposed to chronic alcohol intake.

J. Funct. Food. 72:104045 (2020)
Verlagsversion Forschungsdaten DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Gut microbiota has been identified as a key player in the development of alcoholic liver disease (ALD). Targeting gut microbiota with probiotic intervention will be an attractive approach to prevent ALD. Here, we investigated the effects of probiotic Bifidobacterium breve ATCC15700 (ATCC15700) on liver injury and gut microbiota in mice exposed to chronic alcohol intake. Our results showed that oral administration of ATCC15700 significantly decreased endotoxemia, maintained immune homeostasis, and alleviated alcohol-induced liver injury. ATCC15700 also promoted intestinal barrier function by enhancing the expressions of tight junction proteins in alcohol-treated mice. Moreover, analysis of gut microbiota showed that ATCC15700 normalized the structure and composition of the alcohol-disrupted gut microbiota. Correlation between gut microbiota and liver injury parameters revealed that specific bacteria, including S24_7, unclassified Clostridiales, Butyricicoccus, Oscillospira, Ruminococcus, Mucispirillum and unclassified Lachnospiraceae, were predominantly associated with ALD. In conclusion, ATCC15700 protected alcohol-exposed mice against liver injury via modulating gut micobiota.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Bifidobacterium Breve Atcc15700 ; Alcoholic Liver Disease ; Immune Homeostasis ; Inflammation ; Intestinal Barrier Function ; Gut Microbiota; Intestinal Permeability; Aldehyde Dehydrogenase; Mouse Model; Injury; Dysbiosis; Inflammation; Protection; Dependence; Probiotics; Enzymes
ISSN (print) / ISBN 1756-4646
e-ISSN 1756-4646
Quellenangaben Band: 72, Heft: , Seiten: , Artikelnummer: 104045 Supplement: ,
Verlag Elsevier
Verlagsort Amsterdam
Begutachtungsstatus Peer reviewed