Explore the words cloud of the Diet-namic project. It provides you a very rough idea of what is the project "Diet-namic" about.
The following table provides information about the project.
|Coordinator Country||Germany [DE]|
|Total cost||1˙499˙695 €|
|EC max contribution||1˙499˙695 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2016-12-01 to 2021-11-30|
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|1||UNIVERSITAETSKLINIKUM HAMBURG-EPPENDORF||DE (HAMBURG)||coordinator||1˙499˙695.00|
'The incidence of chronic immune-mediated inflammatory diseases is continually increasing. Chronic inflammation has been linked to intestinal carcinogenesis, which is the second leading cause of cancer-related deaths. The cause of this increase could be the unprecedented dietary abundance typical of “Western” countries. Different types of diets shape the genetic composition and metabolic activity of human intestinal microorganisms; microbiota. There is a continuous cross talk between the microbiota and the immune system. For these reasons, the hypothesis that a “bad” diet promotes a chronic state of intestinal inflammation by shaping the microbiota and in turn carcinogenesis could be supported. However, this hypothesis and whether this is a reversible process remain to be tested.
It has recently been shown that the composition and metabolism of the microbiota is plastic and it can be rapidly “reprogrammed” by switching to a healthier diet. This plastic behaviour has also been attributed to T helper cells. We have shown that Th17 cells, originally thought to be a stable T helper linage, can convert into a more pathogenic phenotype contributing to chronic inflammation or can acquire regulatory functions promoting the resolution of the inflammation.
This project aims to reveal whether mouse and human Th17 cells can quickly adapt to the microbiota as the microbiota does to the diet and in turn mediate the diet effects. By using a unique set of sophisticated transgenic mice we will also test whether the immune system can be corrected by a “simple” change in diet – a widely held belief not yet substantiated.
Studying the potential 'synchronized ballet' of the diet and the immune system will reveal both the enormous dynamism and the revolutionary therapeutic opportunities intrinsic to T cell biology. This project will furthermore identify molecular targets for pharmacological treatments to reverse inflammatory diseases when a simple diet change no longer suffices.'
|year||authors and title||journal||last update|
Francesco Siracusa, Nicola Schaltenberg, Eduardo J. Villablanca, Samuel Huber, Nicola Gagliani
Dietary Habits and Intestinal Immunity: From Food Intake to CD4+ TH Cells
published pages: , ISSN: 1664-3224, DOI: 10.3389/fimmu.2018.03177
|Frontiers in Immunology 9||2019-08-29|
Leonie Brockmann, Shiwa Soukou, Babett Steglich, Paulo Czarnewski, Lilan Zhao, Sandra Wende, Tanja Bedke, Can Ergen, Carolin Manthey, Theodora Agalioti, Maria Geffken, Oliver Seiz, Sara M. Parigi, Chiara Sorini, Jens Geginat, Keishi Fujio, Thomas Jacobs, Thomas Roesch, Jacob R. Izbicki, Ansgar W. Lohse, Richard A. Flavell, Christian Krebs, Jan-Ake Gustafsson, Per Antonson, Maria Grazia Roncarolo,
Molecular and functional heterogeneity of IL-10-producing CD4+ T cells
published pages: , ISSN: 2041-1723, DOI: 10.1038/s41467-018-07581-4
|Nature Communications 9/1||2019-08-29|
Mario Witkowski, Marco Witkowski, Nicola Gagliani, Samuel Huber
Recipe for IBD: can we use food to control inflammatory bowel disease?
published pages: 145-156, ISSN: 1863-2297, DOI: 10.1007/s00281-017-0658-5
|Seminars in Immunopathology 40/2||2019-06-13|
Jan Kempski, Leonie Brockmann, Nicola Gagliani, Samuel Huber
TH17 Cell and Epithelial Cell Crosstalk during Inflammatory Bowel Disease and Carcinogenesis
published pages: , ISSN: 1664-3224, DOI: 10.3389/fimmu.2017.01373
|Frontiers in Immunology 8||2019-06-13|
Theodora Agalioti, Eduardo J. Villablanca, Samuel Huber, Nicola Gagliani
T H 17â€¯cell plasticity: The role of dendritic cells and molecular mechanisms
published pages: 50-60, ISSN: 0896-8411, DOI: 10.1016/j.jaut.2017.12.003
|Journal of Autoimmunity 87||2019-08-29|
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