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InflamCellDeath SIGNED

Mechanism and function of gasdermin-induced inflammatory cell death

Total Cost €


EC-Contrib. €






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

Project "InflamCellDeath" data sheet

The following table provides information about the project.


Organization address
address: Quartier Unil-Centre Bâtiment Unicentre
postcode: 1015

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


Take a look of project's partnership.

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


 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.


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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