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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.

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

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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