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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.

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

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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