Cited by 1,445Inflammasome and immune disordersImmune Response and InflammationCell death mechanisms and regulation

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Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration

Pétrilli, V, Papin, S, Dostert, C, Mayor, A, Martinon, F, Tschopp, J·2007·Cell Death & Differentiation

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Abstract

Inflammasomes are Nod-like receptor(NLR)- and caspase-1-containing cytoplasmic multiprotein complexes, which upon their assembly, process and activate the proinflammatory cytokines interleukin (IL)-1beta and IL-18. The inflammasomes harboring the NLR members NALP1, NALP3 and IPAF have been best characterized. While the IPAF inflammasome is activated by bacterial flagellin, activation of the NALP3 inflammasome is triggered not only by several microbial components, but also by a plethora of danger-associated host molecules such as uric acid. How NALP3 senses these chemically unrelated activators is not known. Here, we provide evidence that activation of NALP3, but not of the IPAF inflammasome, is blocked by inhibiting K(+) efflux from cells. Low intracellular K(+) is also a requirement for NALP1 inflammasome activation by lethal toxin of Bacillus anthracis. In vitro, NALP inflammasome assembly and caspase-1 recruitment occurs spontaneously at K(+) concentrations below 90 mM, but is prevented at higher concentrations. Thus, low intracellular K(+) may be the least common trigger of NALP-inflammasome activation.

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Authors: Pétrilli, V, Papin, S., Dostert, C., Mayor, A., Martinon, F., & Tschopp, J.
Affiliations: University of Lausanne (CH)
Harvard University (US)
Corresponding author: Tschopp, J
ORCID: Pétrilli, V
Papin, S
Martinon, F
Venue: Cell Death & Differentiation
Publisher: Springer Science and Business Media LLC
Published: 2007-06-29
Volume: 14
Issue: 9
Pages: 1583-1589
ISSN: 1350-9047 (ISSN-L)
1476-5403
DOI: 10.1038/sj.cdd.4402195
OpenAlex: W1978274182
Cited by: 1,445
References: 38
Citations by year: 2026: 36 · 2025: 54 · 2024: 62 · 2023: 71 · 2022: 85 · 2021: 78 · 2020: 102 · 2019: 86 · 2018: 73 · 2017: 104 · 2016: 70 · 2015: 79 · 2014: 90 · 2013: 101 · 2012: 93
FWCI: 25.01
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Cell Death and Differentiation (publishedVersion)
PubMed (publishedVersion)
IRIS (submittedVersion)
SERVAL (Université de Lausanne) (submittedVersion)
Funders: National Science Foundation
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: NLRP3 inflammasome, potassium efflux, intracellular potassium concentration, caspase-1 activation, inflammasome assembly, NOD-like receptors, damage-associated molecular patterns, uric acid, IL-1β, IL-18
MeSH terms: NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Calcium-Binding Proteins, Carrier Proteins, Cell Line, Humans, Inflammation, Mice, Inbred BALB C, Mice, Inbred C57BL, Potassium, Macrophages, Peritoneal, Caspase 1, Interleukin-18, Apoptosis Regulatory Proteins, Mice, CARD Signaling Adaptor Proteins, Interleukin-1beta

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Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration

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