MBOAT7 rs641738 increases risk of liver inflammation and transition to fibrosis in chronic hepatitis C

Khaled Thabet, Anastasia Asimakopoulos, Maryam Shojaei, Manuel Romero-Gomez, Alessandra Mangia, William L. Irving, Thomas Berg, Gregory J. Dore, Henning Grønbæk, David Sheridan, Maria Lorena Abate, Elisabetta Bugianesi, Martin Weltman, Lindsay Mollison, Wendy Cheng, Stephen Riordan, Janett Fischer, Ulrich Spengler, Jacob Nattermann, Ahmed Wahid, Angela Rojas, Rose White, Mark W. Douglas, Duncan McLeod, Elizabeth Powell, Christopher Liddle, David van der Poorten, Jacob George () and Mohammed Eslam
Additional contact information
Khaled Thabet: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
Anastasia Asimakopoulos: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
Maryam Shojaei: Centre for Immunology and Allergy Research, Westmead Institute for Medical Research
Manuel Romero-Gomez: Unit for The Clinical Management of Digestive Diseases and CIBERehd, Hospital Universitario de Valme
Alessandra Mangia: Ospedale Casa Sollievo della Sofferenza, IRCCS
William L. Irving: NIHR Biomedical Research Unit in Gastroenterology and the Liver, University of Nottingham
Thomas Berg: Section of Hepatology, Clinic for Gastroenterology and Rheumatology, University Clinic Leipzig
Gregory J. Dore: Kirby Institute, The University of New South Wales
Henning Grønbæk: Aarhus University Hospital
David Sheridan: Institute of Translational and Stratified Medicine, Plymouth University
Maria Lorena Abate: University of Turin
Elisabetta Bugianesi: University of Turin
Martin Weltman: Nepean Hospital
Lindsay Mollison: Fremantle Hospital
Wendy Cheng: Royal Perth Hospital
Stephen Riordan: Gastrointestinal and Liver Unit, Prince of Wales Hospital and University of New South Wales
Janett Fischer: Section of Hepatology, Clinic for Gastroenterology and Rheumatology, University Clinic Leipzig
Ulrich Spengler: University of Bonn
Jacob Nattermann: University of Bonn
Ahmed Wahid: Faculty of Pharmacy, Minia University
Angela Rojas: Unit for The Clinical Management of Digestive Diseases and CIBERehd, Hospital Universitario de Valme
Rose White: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
Mark W. Douglas: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
Duncan McLeod: Institute of Clinical Pathology and Medical Research (ICPMR), Westmead Hospital
Elizabeth Powell: Princess Alexandra Hospital, School of Medicine, The University of Queensland
Christopher Liddle: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
David van der Poorten: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
Jacob George: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney
Mohammed Eslam: Storr Liver Centre, Westmead Institute for Medical Research and Westmead Hospital, University of Sydney

Nature Communications, 2016, vol. 7, issue 1, 1-8

Abstract: Abstract Cirrhosis likely shares common pathophysiological pathways despite arising from a variety of liver diseases. A recent GWAS identified rs641738, a polymorphism in the MBOAT7 locus, as being associated with the development of alcoholic cirrhosis. Here we explore the role of this variant on liver inflammation and fibrosis in two cohorts of patients with chronic hepatitis C. In 2,051 patients, rs641738 associated with severe hepatic inflammation and increased risk of fibrosis, as well as fast fibrosis progression. At functional level, rs641738 associated with MBOAT7 transcript and protein levels in liver and blood, and with serum inflammatory, oxidative stress and macrophage activation markers. MBOAT7 was expressed in immune cell subsets, implying a role in hepatic inflammation. We conclude that the MBOAT7 rs641738 polymorphism is a novel risk variant for liver inflammation in hepatitis C, and thereby for liver fibrosis.

Date: 2016
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DOI: 10.1038/ncomms12757

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