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HepatoMetaboPath SIGNED

Cellular and molecular mechanisms of metabolic immune activation triggering non-alcoholic steatohepatitis (NASH) and HCC

Total Cost €

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EC-Contrib. €

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Partnership

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 HepatoMetaboPath project word cloud

Explore the words cloud of the HepatoMetaboPath project. It provides you a very rough idea of what is the project "HepatoMetaboPath" about.

model    cd8    cancer    nash    hepatocyte    trend    death    usa    overweight    diseases    nkt    cd8t    therapies    antigen    efficacious    recapitulating    demonstrated    expertise    syndrome    found    pathology    reduce    mechanisms    pandemic    genetic    activation    pathogen    suffices    lipid    clinically    transition    inflammation    identical    relevance    disease    subsequent    hepatitis    first    manifest    countries    molecular    dimensions    lacking    significantly    hepatocellular    determinants    cells    hepatocytes    former    time    hepatic    mouse    fibrosis    profile    fatty    world    liver    immune    cell    steatohepatitis    types    unknown    cross    metabolism    recognition    context    frequent    environmental    reaching    rising    clinical    poorly    group    human    normalization    danger    underlining    carcinoma    activated    natural    alcoholic    alter    underlying    viruses    nafld    crosstalk    priming    talk    patients    metabolic    killer    hcc    patterns    industrialized    causing   

Project "HepatoMetaboPath" data sheet

The following table provides information about the project.

Coordinator
HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH 

Organization address
address: INGOLSTADTER LANDSTRASSE 1
city: NEUHERBERG
postcode: 85764
website: www.helmholtz-muenchen.de

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Total cost 1˙995˙860 €
 EC max contribution 1˙995˙860 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-CoG
 Funding Scheme ERC-COG
 Starting year 2016
 Duration (year-month-day) from 2016-07-01   to  2021-06-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH DE (NEUHERBERG) coordinator 1˙995˙860.00

Map

 Project objective

Overweight and metabolic syndrome are reaching pandemic dimensions in industrialized countries and are rising in developing countries. Clinically these diseases can manifest in non-alcoholic fatty liver disease (NAFLD), the most frequent liver disease world-wide. A significant number of NAFLD patients develop non-alcoholic steatohepatitis (NASH), fibrosis and hepatocellular carcinoma (HCC), making NASH-driven HCC the most rapidly increasing cancer in the USA, with a similar trend in Europe. While HCC is the second most common cause of cancer related death, the mechanisms triggering NASH and subsequent HCC are poorly understood and efficacious therapies are lacking. My group has strong expertise in inflammation-driven HCC (e.g. by Hepatitis B, C viruses). Recently, we have established a mouse model of NASH-driven HCC recapitulating human pathology in the context of metabolic syndrome. We demonstrated for the first time that CD8 T- and natural killer T (NKT)-cells become activated during metabolic syndrome, cross-talk with hepatocytes and alter hepatic lipid metabolism causing NASH and HCC. We found an identical profile of CD8T and NKT-cell activation in human NASH underlining the clinical relevance of our model. As the mechanisms of immune cell activation in NASH and transition to HCC remain unknown, this research proposal aims to (1) Identify the priming cell types in metabolic CD8 T-, NKT-cell activation and the molecular mechanisms of immune cell-hepatocyte crosstalk. (2) Determine the role of antigen recognition and danger- or pathogen-associated molecular patterns in NASH/HCC. (3) Identify the environmental and genetic determinants of NASH to HCC transition. Our findings will enhance the understanding of NASH and HCC development by identifying the underlying mechanisms of immune cell activation. We will identify genetic changes facilitating NASH to HCC transition and whether metabolic normalization of former NASH patients suffices to significantly reduce HCC.

 Publications

year authors and title journal last update
List of publications.
2018 Anna Lorentzen, Paul F. Becker, Jan Kosla, Massimo Saini, Kathrin Weidele, Paolo Ronchi, Corinna Klein, Monika J. Wolf, Felix Geist, Bastian Seubert, Marc Ringelhan, Daniela Mihic-Probst, Knud Esser, Marko Roblek, Felix Kuehne, Gaia Bianco, Tracy O’Connor, Quentin Müller, Kathleen Schuck, Sebastian Lange, Daniel Hartmann, Saskia Spaich, Olaf Groß, Jochen Utikal, Sebastian Haferkamp, Martin R.
Single cell polarity in liquid phase facilitates tumour metastasis
published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-018-03139-6
Nature Communications 9/1 2019-09-02
2019 Quentin M. Anstee, Helen L. Reeves, Elena Kotsiliti, Olivier Govaere, Mathias Heikenwalder
From NASH to HCC: current concepts and future challenges
published pages: 411-428, ISSN: 1759-5045, DOI: 10.1038/s41575-019-0145-7
Nature Reviews Gastroenterology & Hepatology 16/7 2019-09-02
2018 Marc Ringelhan, Dominik Pfister, Tracy O’Connor, Eli Pikarsky, Mathias Heikenwalder
The immunology of hepatocellular carcinoma
published pages: 222-232, ISSN: 1529-2908, DOI: 10.1038/s41590-018-0044-z
Nature Immunology 19/3 2019-09-02

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