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Abstract Details
Targeting the gut-liver-immune axis to treat cirrhosis
Gut. 2020 Oct 15;gutjnl-2020-320786. doi: 10.1136/gutjnl-2020-320786.Online ahead of print.
Thomas Henry Tranah1, Lindsey A Edwards1, Bernd Schnabl2, Debbie Lindsay Shawcross3
Author information
1Institute of Liver Studies, Department of Inflammation Biology, School of Immunology and Microbial Sciences, FoLSM, King's College London, London, UK.
2Medicine, University of California San Diego, San Diego, California, USA.
3Institute of Liver Studies, Department of Inflammation Biology, School of Immunology and Microbial Sciences, FoLSM, King's College London, London, UK debbie.shawcross@kcl.ac.uk.
Abstract
Cirrhotic portal hypertension is characterised by development of the decompensating events of ascites, encephalopathy, portal hypertensive bleeding and hepatorenal syndrome, which arise in a setting of cirrhosis-associated immune dysfunction (CAID) and define morbidity and prognosis. CAID describes the dichotomous observations that systemic immune cells are primed and display an inflammatory phenotype, while failing to mount robust responses to pathogen challenge. Bacterial infections including spontaneous bacterial peritonitis are common complications of advanced chronic liver disease and can precipitate variceal haemorrhage, hepatorenal syndrome and acute-on-chronic liver failure; they frequently arise from gut-derived organisms and are closely linked with dysbiosis of the commensal intestinal microbiota in advanced chronic liver disease.Here, we review the links between cirrhotic dysbiosis, intestinal barrier dysfunction and deficits of host-microbiome compartmentalisation and mucosal immune homoeostasis that occur in settings of advanced chronic liver disease. We discuss established and emerging therapeutic strategies targeted at restoring intestinal eubiosis, augmenting gut barrier function and ameliorating the mucosal and systemic immune deficits that characterise and define the course of decompensated cirrhosis.