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5. Heterogeneity of fibrosis patterns in non-alcoholic fatty liver disease supports the presence of multiple fibrogenic pathways

Author

Skoien, Richard, Richardson, Michelle M., Jonsson, Julie R., Powell, Elizabeth E., Brunt, Elizabeth M., Neuschwander-Tetri, Brent A., Bhathal, Prithi S., Dixon, John B., OʼBrien, Paul E., Tilg, Herbert, Moschen, Alexander R., Baumann, Ulrich, Brown, Rachel M., Couper, Richard T., Manton, Nicholas D., Ee, Looi C., Weltman, Martin, and Clouston, Andrew D.

Published
2013
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11. IFN-λ3, not IFN-λ4, likely mediates IFNL3–IFNL4 haplotype–dependent hepatic inflammation and fibrosis

Author

Eslam, Mohammed, McLeod, Duncan, Kelaeng, Kebitsaone Simon, Mangia, Alessandra, Berg, Thomas, Thabet, Khaled, Irving, William, Dore, Gregory J., Sheridan, David, Grønbæk, Henning, Abate, María Lorena, Hartmann, Rune, Bugianesi, Elisabetta, Spengler, Ulrich, Rojas Álvarez-Ossorio, M. Ángeles, Booth, David R., Weltman, Martin, Mollison, Lindsay, Cheng, Wendy, Riordan, Stephen, Mahajan, Hema, Fischer, Janett, Nattermann, Jacob, Douglas, Mark W., Liddle, Christopher, Powell, Elizabeth, Romero-Gómez, Manuel, George, Jacob, Metwally, Mayada, White, Rosa, Gallego-Durán, Rocío, Leung, Reynold, Mahajan, Neha, Bassendine, Margaret, Rahme, Antony, Rosso, Chiara, Mezzabotta, Lavinia, Malik, Barbara, Matthews, Gail, Asimakopoulos, Anastasia, Applegate, Tanya, Grebely, Jason, Fragomeli, Vicenzo, Jonsson, Julie R., Santoro, Rosanna, Sydney Medical Foundation, University of Sydney, and National Health and Medical Research Council (Australia)

Subjects
0301 basic medicine, LAMBDA 4, Genotype, health care facilities, manpower, and services, education, Inflammation, Hepacivirus, LIVER FIBROSIS, GENOME-WIDE-ASSOCIATION, Biology, Polymorphism, Single Nucleotide, Linkage Disequilibrium, INTERFERON-STIMULATED GENES, 03 medical and health sciences, Immune system, Gene Frequency, Fibrosis, INFECTION, Genetics, medicine, Humans, HCV CLEARANCE, SNP, C VIRUS, health care economics and organizations, Hepatitis, Reverse Transcriptase Polymerase Chain Reaction, Interleukins, Haplotype, medicine.disease, Hepatitis C, Phenotype, III INTERFERONS, Logistic Models, 030104 developmental biology, Haplotypes, Liver, Multivariate Analysis, Immunology, SOLID-ORGAN, Interferons, medicine.symptom, IL28B GENE
Abstract

The International Liver Disease Genetics Consortium (ILDGC)., Genetic variation in the IFNL3–IFNL4 (interferon-λ3–interferon-λ4) region is associated with hepatic inflammation and fibrosis1,2,3,4. Whether IFN-λ3 or IFN-λ4 protein drives this association is not known. We demonstrate that hepatic inflammation, fibrosis stage, fibrosis progression rate, hepatic infiltration of immune cells, IFN-λ3 expression, and serum sCD163 levels (a marker of activated macrophages) are greater in individuals with the IFNL3–IFNL4 risk haplotype that does not produce IFN-λ4, but produces IFN-λ3. No difference in these features was observed according to genotype at rs117648444, which encodes a substitution at position 70 of the IFN-λ4 protein and reduces IFN-λ4 activity, or between patients encoding functionally defective IFN-λ4 (IFN-λ4–Ser70) and those encoding fully active IFN-λ4–Pro70. The two proposed functional variants (rs368234815 and rs4803217)5,6 were not superior to the discovery SNP rs12979860 with respect to liver inflammation or fibrosis phenotype. IFN-λ3 rather than IFN-λ4 likely mediates IFNL3–IFNL4 haplotype–dependent hepatic inflammation and fibrosis., M.E., M.D., and J.G. are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney, and by a National Health and Medical Research Council of Australia (NHMRC) Program Grant (1053206) and NHMRC Project Grants (APP1107178 and APP1108422). G.D. is supported by an NHMRC Fellowship (1028432).

Published
2017

30. Diverse impacts of the rs58542926 E167K variant in TM6SF2 on viral and metabolic liver disease phenotypes

Author

Eslam, Mohammed, Mangia, Alessandra, Berg, Thomas, Chan, Henry Lik Yuen, Irving, William L., Dore, Gregory J., Abate, Maria Lorena, Bugianesi, Elisabetta, Adams, Leon A., Najim, Mustafa A. M., Miele, Luca, Weltman, Martin, Mollison, Lindsay, Cheng, Wendy, Riordan, Stephen, Fischer, Janett, Romero Gomez, Manuel, Spengler, Ulrich, Nattermann, Jacob, Rahme, Antony, Sheridan, David, Booth, David R., Mcleod, Duncan, Powell, Elizabeth, Liddle, Christopher, Douglas, Mark W., van der Poorten, David, George, Jacob, White, Rose, Rojas, Angela, Gallego Duran, Rocio, Bassendine, Margaret, Wong, Vincent W. S., Rosso, Chiara, Mezzabotta, Lavinia, Leung, Reynold, Malik, Barbara, Matthews, Gail, Applegate, Tanya, Grebely, Jason, Fragomeli, Vincenzo, Jonsson, Julie R., and Santaro, Rosanna

Subjects
0301 basic medicine, Adult, Male, medicine.medical_specialty, Hepatitis, Viral, Human, Biology, Polymorphism, Single Nucleotide, Cohort Studies, 03 medical and health sciences, Liver disease, 0302 clinical medicine, Non-alcoholic Fatty Liver Disease, Internal medicine, Nonalcoholic fatty liver disease, medicine, Humans, Genetic Predisposition to Disease, Hepatitis, Hepatology, Membrane Proteins, Middle Aged, Viral Load, medicine.disease, Lipid Metabolism, Virology, Fibrosis, 030104 developmental biology, Liver, Case-Control Studies, Immunology, 030211 gastroenterology & hepatology, Female, Steatosis, Viral hepatitis, Viral load, TM6SF2
Abstract

A genome-wide exome association study has identified the transmembrane 6 superfamily member 2 (TM6SF2) rs58542926 variant encoding an E167K substitution as a genetic determinant of hepatic steatosis in nonalcoholic fatty liver disease (NAFLD). The roles of this variant across a spectrum of liver diseases and pathologies and on serum lipids comparing viral hepatitis to NAFLD and viral load in chronic viral hepatitis, as well as its intrahepatic molecular signature, have not been well characterized. We undertook detailed analyses in 3260 subjects with viral and nonviral liver diseases and in healthy controls. Serum inflammatory markers and hepatic expression of TM6SF2 and genes regulating lipid metabolism were assessed in a subset with chronic hepatitis C (CHC). The rs58542926 T allele was more prevalent in 502 NAFLD patients than controls (P = 0.02) but not different in cohorts with CHC (n = 2023) and chronic hepatitis B (n = 507). The T allele was associated with alterations in serum lipids and hepatic steatosis in all diseases and with reduced hepatic TM6SF2 and microsomal triglyceride transfer protein expression. Interestingly, the substitution was associated with reduced CHC viral load but increased hepatitis B virus DNA. The rs58542926 T allele had no effect on inflammation, impacted ≥F2 fibrosis in CHC and NAFLD assessed cross-sectionally (odds ratio = 1.39, 95% confidence interval 1.04-1.87, and odds ratio = 1.62, 95% confidence interval 1.03-2.52, respectively; P0.03 for both), but had no effect on fibrosis progression in 1174 patients with CHC and a known duration of infection.The TM6SF2 E167K substitution promotes steatosis and lipid abnormalities in part by altering TM6SF2 and microsomal triglyceride transfer protein expression and differentially impacts CHC and chronic hepatitis B viral load, while effects on fibrosis are marginal. (Hepatology 2016;64:34-46).

Published
2016

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

Author

Thabet, Khaled, Asimakopoulos, Anastasia, Shojaei, Maryam, Romero Gomez, Manuel, Mangia, Alessandra, Irving, William L., Berg, Thomas, Dore, Gregory J., Grønbæk, Henning, Sheridan, David, Abate, Maria Lorena, Bugianesi, Elisabetta, Weltman, Martin, Mollison, Lindsay, Cheng, Wendy, Riordan, Stephen, Fischer, Janett, Spengler, Ulrich, Nattermann, Jacob, Wahid, Ahmed, Rojas, Angela, White, Rose, Douglas, Mark W., Mcleod, Duncan, Powell, Elizabeth, Liddle, Christopher, Van Der Poorten, David, George, Jacob, Eslam, Mohammed, Gallego Duran, Rocio, Applegate, Tanya, Bassendine, Margaret, Rosso, Chiara, Mezzabotta, Lavinia, Leung, Reynold, Malik, Barbara, Matthews, Gail, Grebely, Jason, Fragomeli, Vincenzo, Jonsson, Julie R., Santaro, Rosanna, Sydney Medical School Foundation, University of Sydney, National Health and Medical Research Council (Australia), Novo Nordisk Foundation, Danish Natural Science Research Council, German Research Foundation, The Hector Foundation, and Egypt Government

Subjects
0301 basic medicine, Liver Cirrhosis, Male, Genetics and Molecular Biology (all), Alcoholic liver disease, Cirrhosis, health care facilities, manpower, and services, General Physics and Astronomy, medicine.disease_cause, Biochemistry, Cohort Studies, Fibrosis, Genetics research, health care economics and organizations, Multidisciplinary, Fatty liver, Liver Neoplasms, Chemistry (all), Hepatitis C, Middle Aged, 3. Good health, Disease Progression, Female, medicine.symptom, Carcinoma, Hepatocellular, Science, Liver fibrosis, education, Inflammation, Polymorphism, Single Nucleotide, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, Physics and Astronomy (all), Immune system, medicine, Journal Article, Humans, business.industry, Membrane Proteins, General Chemistry, Hepatitis C, Chronic, Macrophage Activation, medicine.disease, Fatty Liver, Oxidative Stress, 030104 developmental biology, Case-Control Studies, Immune System, Immunology, Biochemistry, Genetics and Molecular Biology (all), business, Oxidative stress, Acyltransferases
Abstract

International Liver Disease Genetics Consortium., 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., M.E., M.W.D. and J.G. are supported by the Robert W. Storr Bequest to the Sydney Medical Foundation, University of Sydney; a National Health and Medical Research Council of Australia (NHMRC) Program Grant (1053206) and Project grants (APP1107178 and APP1108422). G.D. is supported by an NHMRC Fellowship (1028432). H.G. received support from The NOVO Nordisk Foundation the Danish Strategic Research Council (10-092797). U.S. and J.N. are supported by DFG SFB-TR57 and the Hector-Foundation (M63). K.T. is supported by Scholarship from the Egyptian government.

Published
2016

32. Portal, but not lobular, macrophages express matrix metalloproteinase-9: association with the ductular reaction and fibrosis in chronic hepatitis C

Author

Gadd, Victoria L., primary, Melino, Michelle, additional, Roy, Sandrine, additional, Horsfall, Leigh, additional, O'Rourke, Peter, additional, Williams, Millicent R., additional, Irvine, Katharine M., additional, Sweet, Matthew J., additional, Jonsson, Julie R., additional, Clouston, Andrew D., additional, and Powell, Elizabeth E., additional

Published
2012
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35. Magnetic resonance imaging and spectroscopy accurately estimate the severity of steatosis provided the stage of fibrosis is considered

Author

McPherson, Stuart, primary, Jonsson, Julie R., additional, Cowin, Gary J., additional, O’Rourke, Peter, additional, Clouston, Andrew D., additional, Volp, Andrew, additional, Horsfall, Leigh, additional, Jothimani, Dinesh, additional, Fawcett, Jonathan, additional, Galloway, Graham J., additional, Benson, Mark, additional, and Powell, Elizabeth E., additional

Published
2009
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39. Progressive Fibrosis in Nonalcoholic Steatohepatitis: Association With Altered Regeneration and a Ductular Reaction

Author

Richardson, Michelle M., primary, Jonsson, Julie R., additional, Powell, Elizabeth E., additional, Brunt, Elizabeth M., additional, Neuschwander–Tetri, Brent A., additional, Bhathal, Prithi S., additional, Dixon, John B., additional, Weltman, Martin D., additional, Tilg, Herbert, additional, Moschen, Alexander R., additional, Purdie, David M., additional, Demetris, Anthony J., additional, and Clouston, Andrew D., additional

Published
2007
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40. Relationship Between Steatosis, Inflammation, and Fibrosis in Chronic Hepatitis C: A Meta-Analysis of Individual Patient Data

Author

Leandro, Gioacchino, primary, Mangia, Alessandra, additional, Hui, Jason, additional, Fabris, Paolo, additional, Rubbia–Brandt, Laura, additional, Colloredo, Guido, additional, Adinolfi, Luigi E., additional, Asselah, Tarik, additional, Jonsson, Julie R., additional, Smedile, Antonina, additional, Terrault, Norah, additional, Pazienza, Valerio, additional, Giordani, Maria Teresa, additional, Giostra, Emiliano, additional, Sonzogni, Aurelio, additional, Ruggiero, Giuseppe, additional, Marcellin, Patrick, additional, Powell, Elizabeth E., additional, George, Jacob, additional, and Negro, Francesco, additional

Published
2006
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41. Steatosis Is a Cofactor in Liver Injury in Hemochromatosis

Author

Powell, Elizabeth E., primary, Ali, Azmat, additional, Clouston, Andrew D., additional, Dixon, Jeannette L., additional, Lincoln, Douglas J., additional, Purdie, David M., additional, Fletcher, Linda M., additional, Powell, Lawrie W., additional, and Jonsson, Julie R., additional

Published
2005
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45. Increased mononuclear cell activation and apoptosis early after human liver transplantation is associated with a reduced frequency of acute rejection

Author

Jonsson, Julie R., primary, Gu, Wenyi, additional, Vanags, Daina M., additional, Bishop, G. Alex, additional, McCaughan, Geoffrey W., additional, Fawcett, Jonathon, additional, Lynch, Stephen V., additional, Balderson, Glenda A., additional, Powell, Elizabeth E., additional, and Clouston, Andrew D., additional

Published
2004
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47. Reply

Author

Clouston, Andrew D, primary, Hickman, Ingrid J, additional, Macdonald, Graeme A, additional, Jonsson, Julie R, additional, and Powell, Elizabeth E, additional

Published
2001
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