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Gut microbiota compositional and functional fingerprint in patients with alcohol use disorder and alcohol‐associated liver disease
Author(s) -
Addolorato Giovanni,
Ponziani Francesca R.,
Dionisi Tommaso,
Mosoni Carolina,
Vassallo Gabriele A.,
Sestito Luisa,
Petito Valentina,
Picca Anna,
Marzetti Emanuele,
Tarli Claudia,
Mirijello Antonio,
Zocco Maria Assunta,
Lopetuso Loris R.,
Antonelli Mariangela,
Rando Maria M.,
Paroni Sterbini Francesco,
Posteraro Brunella,
Sanguinetti Maurizio,
Gasbarrini Antonio
Publication year - 2020
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/liv.14383
Subject(s) - medicine , gut flora , bacteroides , gastroenterology , liver disease , alcohol , alcoholic liver disease , microbiome , cirrhosis , immunology , biology , bioinformatics , biochemistry , genetics , bacteria
Background & aims Alcohol use disorder (AUD) represents the most common cause of liver disease. The gut microbiota plays a critical role in the progression of alcohol‐related liver damage. Aim of this study was to characterize the gut microbial composition and function in AUD patients with alcohol‐associated liver disease (AALD). Methods This study included 36 AUD patients (14 with cirrhosis) who were active drinkers and an equal number of matched controls. Stool microbial composition, serum levels of lipopolysaccharide, cytokines/chemokines and gut microbiota functional profile were assessed. Results AUD patients had a decreased microbial alpha diversity as compared to controls (0.092 vs 0.130, P = .047) and a specific gut microbial signature. The reduction of Akkermansia and the increase in Bacteroides were able to identify AUD patients with an accuracy of 93.4%. Serum levels of lipopolysaccharide (4.91 vs 2.43, P = .009) and pro‐inflammatory mediators (tumour necrosis factor alpha 60.85 vs 15.08, P = .001; interleukin [IL] 1beta 4.43 vs 1.72, P = .0001; monocyte chemoattractant protein 1 225.22 vs 16.43, P = .006; IL6 1.87 vs 1.23, P = .008) were significantly increased in AUD patients compared to controls and in cirrhotic patients compared to non‐cirrhotic ones (IL6 3.74 vs 1.39, P = .019; IL8 57.60 vs 6.53, P = .004). The AUD‐associated gut microbiota showed an increased expression of gamma‐aminobutyric acid (GABA) metabolic pathways and energy metabolism. Conclusions AUD patients present a specific gut microbial fingerprint, associated with increased endotoxaemia, systemic inflammatory status and functional alterations that may be involved in the progression of the AALD and in the pathogenesis of AUD.