Hepatic encephalopathy (HE) is a debilitating neuropsychiatric condition often associated with acute liver failure or cirrhosis. Advanced liver diseases are characterized by a leaky gut and systemic inflammation. There is strong evidence that the pathogenesis of HE is linked to a dysbiotic gut microbiota and to harmful microbial by-products, such as ammonia, indoles, oxindoles and endotoxins. Increased concentrations of these toxic metabolites together with the inability of the diseased liver to clear such products is thought to play an important patho-ethiological role. Current first line clinical treatments target microbiota dysbiosis by decreasing the counts of pathogenic bacteria, blood endotoxemia and ammonia levels. This review will focus on the role of the gut microbiota and its metabolism in HE and advanced cirrhosis. It will critically assess data from different clinical trials measuring the efficacy of the prebiotic lactulose, the probiotic VSL#3 and the antibiotic rifaximin in treating HE and advanced cirrhosis, through gut microbiota modulation. Additionally data from Randomised Controlled Trials using pre-, pro- and synbiotic will be also considered by reporting meta-analysis studies. The large amount of existing data showed that HE is a clear example of how an altered gut microbiota homeostasis can influence and impact on physiological functions outside the intestine, with implication for host health at the systems level. Nevertheless, a strong effort should be made to increase the information on gut microbiota ecology and its metabolic function in liver diseases and HE.

Mancini, A.; Campagna, F.; Amodio, P.; Tuohy, K. (2018). Gut : liver : brain axis: the microbial challenge in the hepatic encephalopathy. FOOD & FUNCTION, 9 (3): 1373-1388. doi: 10.1039/C7FO01528C handle: http://hdl.handle.net/10449/46458

Gut : liver : brain axis: the microbial challenge in the hepatic encephalopathy

Mancini, A.
Primo
;
Tuohy, K.
Ultimo
2018-01-01

Abstract

Hepatic encephalopathy (HE) is a debilitating neuropsychiatric condition often associated with acute liver failure or cirrhosis. Advanced liver diseases are characterized by a leaky gut and systemic inflammation. There is strong evidence that the pathogenesis of HE is linked to a dysbiotic gut microbiota and to harmful microbial by-products, such as ammonia, indoles, oxindoles and endotoxins. Increased concentrations of these toxic metabolites together with the inability of the diseased liver to clear such products is thought to play an important patho-ethiological role. Current first line clinical treatments target microbiota dysbiosis by decreasing the counts of pathogenic bacteria, blood endotoxemia and ammonia levels. This review will focus on the role of the gut microbiota and its metabolism in HE and advanced cirrhosis. It will critically assess data from different clinical trials measuring the efficacy of the prebiotic lactulose, the probiotic VSL#3 and the antibiotic rifaximin in treating HE and advanced cirrhosis, through gut microbiota modulation. Additionally data from Randomised Controlled Trials using pre-, pro- and synbiotic will be also considered by reporting meta-analysis studies. The large amount of existing data showed that HE is a clear example of how an altered gut microbiota homeostasis can influence and impact on physiological functions outside the intestine, with implication for host health at the systems level. Nevertheless, a strong effort should be made to increase the information on gut microbiota ecology and its metabolic function in liver diseases and HE.
Settore BIO/19 - MICROBIOLOGIA GENERALE
2018
Mancini, A.; Campagna, F.; Amodio, P.; Tuohy, K. (2018). Gut : liver : brain axis: the microbial challenge in the hepatic encephalopathy. FOOD & FUNCTION, 9 (3): 1373-1388. doi: 10.1039/C7FO01528C handle: http://hdl.handle.net/10449/46458
File in questo prodotto:
File Dimensione Formato  
2018 FF.pdf

solo utenti autorizzati

Licenza: Tutti i diritti riservati (All rights reserved)
Dimensione 692.84 kB
Formato Adobe PDF
692.84 kB Adobe PDF   Visualizza/Apri   Richiedi una copia

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10449/46458
Citazioni
  • ???jsp.display-item.citation.pmc??? 30
  • Scopus 57
  • ???jsp.display-item.citation.isi??? 50
social impact