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BILITOLERANCE SIGNED

Control of disease tolerance to infection by Biliverdin Reductase A

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 BILITOLERANCE project word cloud

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

tested    trade    ferritin    deleterious    of    fitness    evolutionary    strategy    clearance    bvra    mechanisms    lipid    characterizing    resistance    effector    carry    oxidative    expression    stress    peroxidation    containment    preserve    ahr    offs    genes    possibly    output    receptor    limits    sequestering    pro    modulate    imposed    conserved    said    iron    chain    pressure    multiple    evolution    tissue    coupled    immune    limit    led    relies    oxygenase    confer    disease    protein    cells    enzyme    pathogen    direct    hydrocarbon    shaped    health    negative    host    infection    resident    bilitolerance    survival    anti    central    biliverdin    parenchyma    compromising    heme    unexplored    primarily    expulsion    provides    activation    immunopathology    conversion    illustrated    mechanism    function    lipophilic    functional    reductase    selective    damage    tolerance    emergence    defense    oxidant    tissues    pathogens    countervailing    aryl    infections    bilirubin    potent    exerting    signals    catabolism    hypothesis    catabolizing    presumably    macrophages   

Project "BILITOLERANCE" data sheet

The following table provides information about the project.

Coordinator
FUNDACAO CALOUSTE GULBENKIAN 

Organization address
address: AVENIDA BERNA 45
city: LISBOA
postcode: 1000
website: www.igc.gulbenkian.pt

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 Portugal [PT]
 Total cost 160˙635 €
 EC max contribution 160˙635 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-12-01   to  2021-02-04

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    FUNDACAO CALOUSTE GULBENKIAN PT (LISBOA) coordinator 160˙635.00

Map

 Project objective

The immune system was shaped through evolution, primarily through the selective pressure imposed by pathogens. This led to the emergence of multiple mechanisms that limit the negative impact of pathogens on host health and fitness. The best recognized defense strategy against infections relies on resistance mechanisms that aim at pathogen containment, expulsion or clearance. While crucial for host survival to infection, resistance mechanisms can carry significant trade-offs, often driven by oxidative stress and damage imposed to host parenchyma cells, and in some cases compromising the functional output of host tissues, i.e. immunopathology. Presumably for this reason, resistance mechanisms are coupled to countervailing oxidative stress responses that preserve parenchyma tissue function. These provide tissue damage control without exerting a direct negative impact on pathogens and as such are said to confer disease tolerance to infection. This defense strategy relies on the expression of a number of evolutionary conserved effector genes controlling the pro-oxidant effects of iron and heme, as illustrated for the heme catabolizing enzyme heme oxygenase 1 or the iron sequestering protein ferritin H chain. BILITOLERANCE aims at identifying and characterizing an unexplored and possibly central component of this tissue damage control mechanism that relies on the conversion of the end-product of heme catabolism biliverdin into bilirubin, by biliverdin reductase A (BVRA). The central hypothesis to be tested by BILITOLERANCE is that bilirubin generated by BVRA provides a potent lipophilic anti-oxidant defense mechanism that limits the deleterious effects of lipid peroxidation. Moreover BILITOLERANCE will test the hypothesis that bilirubin also signals via the aryl hydrocarbon receptor (AhR) to modulate the activation of tissue-resident macrophages and promote tissue damage control and disease tolerance to infection.

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

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