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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.

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

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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