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InflamCellDeath SIGNED

Mechanism and function of gasdermin-induced inflammatory cell death

Total Cost €

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EC-Contrib. €

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Partnership

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 InflamCellDeath project word cloud

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

death    cleavage    pores    comprehensively    substances    receptors    family    function    forming    detection    proteases    therapies    cytokines    membrane    repair    innate    danger    characterizing    members    protein    cytosolic    gasdermin    inflammatory    infectious    pro    group    bacterial    single    signals    lytic    cytotoxic    defense    assembled    concomitant    promotes    antimicrobial    platforms    infection    recognition    dependent    causes    appear    restricting    effectors    signalling    permeability    cell    elucidate    regulators    gasdermins    necrotic    pattern    regulation    pyroptosis    injury    activation    caspases    caspase    share    fragment    found    pathogen    noxious    larger    programmed    caused    generates    chronic    host    immune    microbial    substrate    terminal    plasma    pore    inflammation    inflammasome    release    detrimental    disease    regulate    activated    pyroptotic    diseases    leaderless    inflammasomes    anti    forms    mechanism   

Project "InflamCellDeath" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE DE LAUSANNE 

Organization address
address: Quartier Unil-Centre Bâtiment Unicentre
city: LAUSANNE
postcode: 1015
website: www.unil.ch

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 Switzerland [CH]
 Total cost 1˙999˙176 €
 EC max contribution 1˙999˙176 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-COG
 Funding Scheme ERC-COG
 Starting year 2018
 Duration (year-month-day) from 2018-03-01   to  2023-02-28

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE LAUSANNE CH (LAUSANNE) coordinator 1˙999˙176.00

Map

 Project objective

Pyroptosis is a lytic pro-inflammatory type of programmed cell death that is induced by inflammatory caspases, a family of proteases that control the innate immune response to infection, injury or noxious substances. Inflammatory caspases are activated within so-called inflammasomes, cytosolic signalling platforms that are assembled by pattern recognition receptors upon the detection of pathogen- or host-derived danger signals. Pyroptosis is essential for antimicrobial host defense, but also promotes the concomitant release of inflammatory danger signals and leaderless cytokines that is detrimental during chronic inflammatory disease.

Recently it was found that pyroptosis is caused by the cleavage of a single caspase substrate called gasdermin-D. This cleavage generates a cytotoxic N-terminal fragment of gasdermin-D that targets the plasma membrane, where it forms large permeability pores and thus causes pyroptotic cell death. Gasdermin-D is only one member of the larger gasdermin protein family, an emerging group of cell death effectors that share its pore-forming cytotoxic activity and that appear to be major regulators of inflammatory necrotic cell death.

The main goal of this proposal is to comprehensively characterize the function of gasdermins in anti-microbial host defense, to investigate the consequences of gasdermin-D pore formation to the host cell and to elucidate the pathways that regulate gasdermin activation. My objectives are:

1) to define the role of gasdermin-D in inflammasome-dependent anti-bacterial host defense 2) to study the role of membrane repair in restricting gasdermin-D-induced membrane 3) to characterize the function and regulation of other gasdermin family members during infection

By characterizing the mechanism and function of gasdermin-induced cell death in host-defense and inflammation this project may contribute to the development of novel therapies for infectious as well as inflammatory diseases.

 Publications

year authors and title journal last update
List of publications.
2018 Sebastian Rühl, Kateryna Shkarina, Benjamin Demarco, Rosalie Heilig, José Carlos Santos, Petr Broz
ESCRT-dependent membrane repair negatively regulates pyroptosis downstream of GSDMD activation
published pages: 956-960, ISSN: 0036-8075, DOI: 10.1126/science.aar7607
Science 362/6417 2019-10-07
2019 Kaiwen W. Chen, Benjamin Demarco, Petr Broz
Pannexin‐1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or noncanonical inflammasome activation
published pages: , ISSN: 0014-2980, DOI: 10.1002/eji.201948254
European Journal of Immunology 2019-10-07
2019 Kaiwen W. Chen, Dave Boucher, Petr Broz
Divide to conquer: NLRP3 is activated on dispersed trans-Golgi network
published pages: 181-182, ISSN: 1001-0602, DOI: 10.1038/s41422-018-0138-z
Cell Research 29/3 2019-10-07
2019 Kaiwen W Chen, Benjamin Demarco, Rosalie Heilig, Kateryna Shkarina, Andreas Boettcher, Christopher J Farady, Pawel Pelczar, Petr Broz
Extrinsic and intrinsic apoptosis activate pannexin‐1 to drive NLRP 3 inflammasome assembly
published pages: , ISSN: 0261-4189, DOI: 10.15252/embj.2019101638
The EMBO Journal 38/10 2019-10-07
2019 Benjamin Demarco, Kaiwen W. Chen, Petr Broz
Pannexin-1 channels bridge apoptosis to NLRP3 inflammasome activation
published pages: 1610324, ISSN: 2372-3556, DOI: 10.1080/23723556.2019.1610324
Molecular & Cellular Oncology 6/4 2019-10-07

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

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