Giovanni Addolorato1,2, Francesca R Ponziani3, Tommaso Dionisi2, Carolina Mosoni2, Gabriele A Vassallo4, Luisa Sestito2, Valentina Petito3, Anna Picca5, Emanuele Marzetti5, Claudia Tarli2, Antonio Mirijello6, Maria Assunta Zocco3, Loris R Lopetuso3, Mariangela Antonelli2, Maria M Rando2, Francesco Paroni Sterbini7, Brunella Posteraro3,8, Maurizio Sanguinetti7,8, Antonio Gasbarrini1,3. 1. Institute of Internal Medicine and Gastroenterology, Catholic University of Rome, Rome, Italy. 2. Alcohol Use Disorder and Alcohol Related Disease Unit, Department of Internal Medicine and Gastroenterology, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. 3. Internal Medicine, Gastroenterology and Hepatology Unit, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. 4. Internal Medicine Department, Barone Lombardo Hospital, Canicattì, Italy. 5. Department of Geriatrics, Neuroscience and Orthopedics, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. 6. Department of Medical Sciences, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo, Italy. 7. Department of Laboratory and Infectious Disease Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy. 8. Institute of Microbiology, Chatoloc University of Rome, Rome, Italy.
Abstract
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.
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 AUDpatients with alcohol-associated liver disease (AALD). METHODS: This study included 36 AUDpatients (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:AUDpatients 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 AUDpatients 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 AUDpatients compared to controls and in cirrhoticpatients 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:AUDpatients 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.
Authors: Antonio Gasbarrini; Maurizio Pompili; Francesca Romana Ponziani; Angela De Luca; Anna Picca; Emanuele Marzetti; Valentina Petito; Federica Del Chierico; Sofia Reddel; Francesco Paroni Sterbini; Maurizio Sanguinetti; Lorenza Putignani Journal: Hepatol Commun Date: 2022-03-09
Authors: Luca Maccioni; Bei Gao; Sophie Leclercq; Boris Pirlot; Yves Horsmans; Philippe De Timary; Isabelle Leclercq; Derrick Fouts; Bernd Schnabl; Peter Stärkel Journal: Gut Microbes Date: 2020-06-26
Authors: Carla B P Silva; Jefferson Elias-Oliveira; Cameron G McCarthy; Camilla F Wenceslau; Daniela Carlos; Rita C Tostes Journal: Am J Physiol Heart Circ Physiol Date: 2021-06-18 Impact factor: 5.125