ArticleCellular microbiology2008
Heat shock inhibits caspase-1 activity while also preventing its inflammasome-mediated activation by anthrax lethal toxin.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Resolution of inflammation in chronic disease via restoration of the heat shock response (HSR).Cell stress & chaperones · 2024Review
- Heat shock response during the resolution of inflammation and its progressive suppression in chronic-degenerative inflammatory diseases.Cell stress & chaperones · 2024Review
- A Preliminary Study of Mild Heat Stress on Inflammasome Activation in Murine Macrophages.Cells · 2023Article
- Innate immunity, inflammation activation and heat-shock protein in COVID-19 pathogenesis.Journal of neuroimmunology · 2021Review
- Suppressed anti-inflammatory heat shock response in high-risk COVID-19 patients: lessons from basic research (inclusive bats), light on conceivable therapies.Clinical science (London, England : 1979) · 2020Review
- Inhibition of HSP90 and Activation of HSF1 Diminish Macrophage NLRP3 Inflammasome Activity in Alcohol-Associated Liver Injury.Alcoholism, clinical and experimental research · 2020Article
- Heat Shock Proteins and Inflammasomes.International journal of molecular sciences · 2019Review
- HSP70 is a negative regulator of NLRP3 inflammasome activation.Cell death & disease · 2019Article
- Article
- The crystal-induced activation of NLRP3 inflammasomes in atherosclerosis.Inflammation and regeneration · 2017Review
- Pro- and anti-inflammatory cytokine responses to a 164-km road cycle ride in a hot environment.European journal of applied physiology · 2016Article
- HSP90 Regulation of P2X7 Receptor Function Requires an Intact Cytoplasmic C-Terminus.Molecular pharmacology · 2016Article
- Sulforaphane inhibits multiple inflammasomes through an Nrf2-independent mechanism.Journal of leukocyte biology · 2016Article
- The cyclopentenone prostaglandin 15d-PGJ2 inhibits the NLRP1 and NLRP3 inflammasomes.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- G Protein signaling modulator-3 inhibits the inflammasome activity of NLRP3.The Journal of biological chemistry · 2014Article
- Arsenic trioxide and other arsenical compounds inhibit the NLRP1, NLRP3, and NAIP5/NLRC4 inflammasomes.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Anthrax and the inflammasome.Microbes and infection · 2012Review
- Anthrax lethal factor cleavage of Nlrp1 is required for activation of the inflammasome.PLoS pathogens · 2012Article
- Auranofin protects against anthrax lethal toxin-induced activation of the Nlrp1b inflammasome.Antimicrobial agents and chemotherapy · 2011Article
- Anthrax lethal toxin activates the inflammasome in sensitive rat macrophages.Biochemical and biophysical research communications · 2010Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Anthrax lethal toxin (LT) rapidly kills macrophages from certain mouse strains in a mechanism dependent on the breakdown of unknown protein(s) by the proteasome, formation of the Nalp1b (NLRP1b) inflammasome and subsequent activation of caspase-1. We report that heat-shocking LT-sensitive macrophages rapidly protects them against cytolysis by inhibiting caspase-1 activation without upstream effects on LT endocytosis or cleavage of the toxin's known cytosolic substrates (mitogen-activated protein kinases). Heat shock protection against LT occurred through a mechanism independent of de novo protein synthesis, HSP90 activity, p38 activation or proteasome inhibition and was downstream of mitogen-activated protein kinase cleavage and degradation of an unknown substrate by the proteasome. The heat shock inhibition of LT-mediated caspase-1 activation was not specific to the Nalp1b (NLRP1b) inflammasome, as heat shock also inhibited Nalp3 (NLRP3) inflammasome-mediated caspase-1 activation in macrophages. We found that heat shock induced pro-caspase-1 association with a large cellular complex that could prevent its activation. Additionally, while heat-shocking recombinant caspase-1 did not affect its activity in vitro, lysates from heat-shocked cells completely inhibited recombinant active caspase-1 activity. Our results suggest that heat shock inhibition of active caspase-1 can occur independently of an inflammasome platform, through a titratable factor present within intact, functioning heat-shocked cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.