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Addendum: MCC950 closes the active conformation of NLRP3 to an inactive state

Ana Tapia-Abellán
Diego Angosto-Bazarra
Pablo Pelegrin
Amendments and Corrections25 Jan 2021
Nature Chemical Biology

Volume: 17, P: 361
The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response

The NLRP3 inflammasome is involved in IL-1 production and pyroptosis. Pelegrín et al. demonstrate that it is also released extracellularly as a functional proinflammatory particle.

Alberto Baroja-Mazo
Fatima Martín-Sánchez
Pablo Pelegrín
Research22 Jun 2014
Nature Immunology

Volume: 15, P: 738-748
P2X7 receptor induces mitochondrial failure in monocytes and compromises NLRP3 inflammasome activation during sepsis

Systemic sepsis is a potentially life-threatening illness and immunocompromised individuals are especially vulnerable. Here, using a cohort of patients with intra-abdominal origin sepsis, the authors show an important role for the NLRP3 inflammasome in establishing a host response, and NLRP3 dysfunction is a common feature of sepsis mortality.

Juan José Martínez-García
Helios Martínez-Banaclocha
Pablo Pelegrin
ResearchOpen Access20 Jun 2019
Nature Communications

Volume: 10, P: 1-14
Pathogenic NLRP3 mutants form constitutively active inflammasomes resulting in immune-metabolic limitation of IL-1β production

Gain-of-function mutations in NLRP3 result in Cryopyrin-Associated Periodic Syndrome in human patients. Here authors show that although these NLRP3 variants are constitutively active, they preserve their responsiveness to external pro-inflammatory stimuli, and they interfere with the immune-metabolic inflammatory pathways in monocytes.

Cristina Molina-López
Laura Hurtado-Navarro
Pablo Pelegrin
ResearchOpen Access06 Feb 2024
Nature Communications

Volume: 15, P: 1-21
Macrophage activation and polarization modify P2X7 receptor secretome influencing the inflammatory process

Carlos de Torre-Minguela
Maria Barberà-Cremades
Pablo Pelegrín
ResearchOpen Access03 Mar 2016
Scientific Reports

Volume: 6, P: 1-11
MCC950 closes the active conformation of NLRP3 to an inactive state

MCC950, a small-molecule inhibitor of the NLRP3 inflammasome, inactivates NLRP3, including hyperactive disease-linked mutations, by closing the ‘open’ conformation, thereby preventing conformational changes required for NLRP3 activation.

Ana Tapia-Abellán
Diego Angosto-Bazarra
Pablo Pelegrin
Research13 May 2019
Nature Chemical Biology

Volume: 15, P: 560-564
Mitochondrial respiratory-chain adaptations in macrophages contribute to antibacterial host defense

Garaude and colleagues show that innate immunological sensing of live bacteria by macrophages elicits transient adaptations to the electron-transport chain of mitochondria.

Johan Garaude
Rebeca Acín-Pérez
David Sancho
Research27 Jun 2016
Nature Immunology

Volume: 17, P: 1037-1045
Involvement of P2X7 receptor in neuronal degeneration triggered by traumatic injury

Francisco M. Nadal-Nicolás
Caridad Galindo-Romero
Marta Agudo-Barriuso
ResearchOpen Access08 Dec 2016
Scientific Reports

Volume: 6, P: 1-14
NLRP3 lacking the leucine-rich repeat domain can be fully activated via the canonical inflammasome pathway

Activation of the NLRP3 inflammasome is associated with various diseases but its activation mechanism is not fully understood. Here, the authors determine the impact of different NLRP3 domains on sensing NLRP3 triggers, inflammasome assembly and regulation of NLRP3 inflammasome activation.

Iva Hafner-Bratkovič
Petra Sušjan
Roman Jerala
ResearchOpen Access05 Dec 2018
Nature Communications

Volume: 9, P: 1-18
SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer

The capacity of cancer cells to migrate is intimately linked to their ability to induce metastasis. Here the authors show that the sodium channel β4 subunit regulates breast cancer cell migration via inhibition of RhoA activation, independently from its function as an auxiliary protein of the sodium channel.

Emeline Bon
Virginie Driffort
Sébastien Roger
ResearchOpen Access05 Dec 2016
Nature Communications

Volume: 7, P: 1-18
Neutrophils mediate Salmonella Typhimurium clearance through the GBP4 inflammasome-dependent production of prostaglandins

The role of guanylate-binding proteins (GBPs) in innate immunity is increasingly recognized. Here the authors show that GBP4 activates inflammasome in zebrafish neutrophils, and that this process is critical for the clearance of Salmonellainfection via prostaglandin D2.

Sylwia D. Tyrkalska
Sergio Candel
Victoriano Mulero
ResearchOpen Access01 Jul 2016
Nature Communications

Volume: 7, P: 1-17
Author Correction: Early endosome autoantigen 1 regulates IL-1β release upon caspase-1 activation independently of gasdermin D membrane permeabilization

Alberto Baroja-Mazo
Vincent Compan
Pablo Pelegrín
Amendments and CorrectionsOpen Access01 Dec 2020
Scientific Reports

Volume: 10, P: 1
The gasdermins, a protein family executing cell death and inflammation

The gasdermin family of proteins has the capacity to form pores in the membrane, causing a pro-inflammatory lytic type of cell death called pyroptosis, This Review provides a comprehensive overview of the gasdermin family, the mechanisms that control their activation and their role in inflammatory disorders and cancer.

Petr Broz
Pablo Pelegrín
Feng Shao
Reviews05 Nov 2019
Nature Reviews Immunology

Volume: 20, P: 143-157
The total electric charge and time of application of galvanic currents to macrophages can optimize the release of IL-1β with low cell death

Alejandro Peñin-Franch
José Antonio García-Vidal
Pablo Pelegrín
ResearchOpen Access28 Dec 2024
Scientific Reports

Volume: 14, P: 1-10
Involvement of the P2X7-NLRP3 axis in leukemic cell proliferation and death

Erica Salaro
Alessia Rambaldi
Francesco Di Virgilio
ResearchOpen Access25 May 2016
Scientific Reports

Volume: 6, P: 1-13
Detection of inflammasome activation in liver tissue during the donation process as potential biomarker for liver transplantation

Sandra V. Mateo
Daniel Vidal-Correoso
Alberto Baroja-Mazo
ResearchOpen Access30 May 2024
Cell Death Discovery

Volume: 10, P: 1-14
Early endosome autoantigen 1 regulates IL-1β release upon caspase-1 activation independently of gasdermin D membrane permeabilization

Alberto Baroja-Mazo
Vincent Compan
Pablo Pelegrín
ResearchOpen Access08 Apr 2019
Scientific Reports

Volume: 9, P: 1-10
Evaluation of the host immune response assay SeptiCyte RAPID for potential triage of COVID-19 patients

Maria Milagro Montero
Max Hardy-Werbin
Juan Pablo Horcajada
ResearchOpen Access18 Jan 2023
Scientific Reports

Volume: 13, P: 1-11
Identification of an ASC oligomerization inhibitor for the treatment of inflammatory diseases

Paula M. Soriano-Teruel
Guillermo García‑Laínez
Mar Orzáez
ResearchOpen Access13 Dec 2021
Cell Death & Disease

Volume: 12, P: 1-11
Extracellular NLRP3 inflammasome particles are internalized by human coronary artery smooth muscle cells and induce pro-atherogenic effects

Susanne Gaul
Karen Marie Schaeffer
Ulrich Laufs
ResearchOpen Access26 Jul 2021
Scientific Reports

Volume: 11, P: 1-13
Lytic cell death induced by melittin bypasses pyroptosis but induces NLRP3 inflammasome activation and IL-1β release

Fátima Martín-Sánchez
Juan José Martínez-García
Pablo Pelegrín
ResearchOpen Access10 Aug 2017
Cell Death & Disease

Volume: 8, P: e2984
Inflammasome-dependent IL-1β release depends upon membrane permeabilisation

F Martín-Sánchez
C Diamond
P Pelegrín
ResearchOpen Access12 Feb 2016
Cell Death & Differentiation

Volume: 23, P: 1219-1231
Physiological and pathophysiological functions of NLRP6: pro- and anti-inflammatory roles

This review discusses emerging roles for the NLR family pyrin domain containing 6 receptor (NLRP6) in intestinal homeostasis, inflammation, cancer, the nervous system and liver disease.

Diego Angosto-Bazarra
Cristina Molina-López
Pablo Pelegrín
ReviewsOpen Access01 Jun 2022
Communications Biology

Volume: 5, P: 1-8

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Addendum: MCC950 closes the active conformation of NLRP3 to an inactive state

The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response

P2X7 receptor induces mitochondrial failure in monocytes and compromises NLRP3 inflammasome activation during sepsis

Pathogenic NLRP3 mutants form constitutively active inflammasomes resulting in immune-metabolic limitation of IL-1β production

Macrophage activation and polarization modify P2X7 receptor secretome influencing the inflammatory process

MCC950 closes the active conformation of NLRP3 to an inactive state

Mitochondrial respiratory-chain adaptations in macrophages contribute to antibacterial host defense

Involvement of P2X7 receptor in neuronal degeneration triggered by traumatic injury

NLRP3 lacking the leucine-rich repeat domain can be fully activated via the canonical inflammasome pathway

SCN4B acts as a metastasis-suppressor gene preventing hyperactivation of cell migration in breast cancer

Neutrophils mediate Salmonella Typhimurium clearance through the GBP4 inflammasome-dependent production of prostaglandins

Author Correction: Early endosome autoantigen 1 regulates IL-1β release upon caspase-1 activation independently of gasdermin D membrane permeabilization

The gasdermins, a protein family executing cell death and inflammation

The total electric charge and time of application of galvanic currents to macrophages can optimize the release of IL-1β with low cell death

Involvement of the P2X7-NLRP3 axis in leukemic cell proliferation and death

Detection of inflammasome activation in liver tissue during the donation process as potential biomarker for liver transplantation

Early endosome autoantigen 1 regulates IL-1β release upon caspase-1 activation independently of gasdermin D membrane permeabilization

Evaluation of the host immune response assay SeptiCyte RAPID for potential triage of COVID-19 patients

Identification of an ASC oligomerization inhibitor for the treatment of inflammatory diseases

Extracellular NLRP3 inflammasome particles are internalized by human coronary artery smooth muscle cells and induce pro-atherogenic effects

Lytic cell death induced by melittin bypasses pyroptosis but induces NLRP3 inflammasome activation and IL-1β release

Inflammasome-dependent IL-1β release depends upon membrane permeabilisation

Physiological and pathophysiological functions of NLRP6: pro- and anti-inflammatory roles

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