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Interspecies hydrogen transfer in the mammalian gut: how interactions between fermenters and hydrogenotrophs influence colonic homeostasis

Total Cost €


EC-Contrib. €






 H2Gut project word cloud

Explore the words cloud of the H2Gut project. It provides you a very rough idea of what is the project "H2Gut" about.

understand    microbial    facilitates    accumulation    functional    colonize    immune    reducing    nutrients    mechanisms    critical    fermenters    enteropathogens    disposed    fermentation    healthy    chain    single    first    members    sulfate    fat    stimulates    controls    disrupts    community    components    acetogens    hydrogen    expressed    acids    srb    cell    gas    guilds    microbiota    actively    microbe    influence    harvesting    buildup    host    elucidate    colonic    consuming    dispersal    producers    drive    prevented    undigested    efficient    fatty    microbes    bioreactor    metabolite    actions    forces    resistance    communities    mammalian    model    methanogens    characterization    transfer    economy    ecological    interactions    human    dietary    insulin    alters    flow    groups    consumers    deposition    situ    duty    physiological    gut    scfas    bacteria    mouse    spatial    carbon    exerts    identity    principal    energy    h2    appetite    harmful    protects    consumption    function   

Project "H2Gut" data sheet

The following table provides information about the project.


Organization address
city: WIEN
postcode: 1010

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 Austria [AT]
 Total cost 178˙156 €
 EC max contribution 178˙156 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-09-01   to  2020-08-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAT WIEN AT (WIEN) coordinator 178˙156.00


 Project objective

The human gut is a complex microbial bioreactor which protects the host from enteropathogens, facilitates the harvesting of nutrients and energy from undigested dietary components, stimulates healthy immune function, alters host insulin resistance, and exerts control over fat deposition and appetite. The principal duty of the bacteria in the mammalian gut is the fermentation of undigested dietary components, which results in the production of short-chain fatty acids (SCFAs) and H2 gas. The H2 produced by fermentation has to be disposed of very efficiently, since the buildup of H2 strongly disrupts gut function. The harmful accumulation of H2 is prevented by three groups of H2-consuming microbes - sulfate-reducing bacteria (SRB), acetogens, and methanogens. Thus, H2 is a critical metabolite in the gut that controls colonic fermentation and the flow of energy and carbon to the host. Yet, we do not understand the identity of the major functional producers/consumers of H2, the ecological forces that drive one or more of the H2-consuming guilds to colonize the gut, or the microbe-microbe interactions between fermenters and H2-consumers that lead to efficient H2 dispersal. The objectives of the proposed research program are to 1) determine what pathways for H2 production and consumption are actively expressed in the gut using a mouse model, 2) elucidate the identity and spatial distribution of hydrogen producers/consumers in the mouse gut at the single cell level, and 3) ) elucidate the physiological mechanisms of H2 transfer in the gut using model communities. Overall, these research actions will produce the first characterization of the microbiota community members that actively influence the hydrogen economy in the gut in-situ and how these microbe-microbe interactions control colonic fermentation.

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The information about "H2GUT" are provided by the European Opendata Portal: CORDIS opendata.

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