ArticleInfection and immunity2016
Shiga Toxins Activate the NLRP3 Inflammasome Pathway To Promote Both Production of the Proinflammatory Cytokine Interleukin-1β and Apoptotic Cell Death.
Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Neuroimmune Regulation of NLRP3 Signalling in Parkinson's Disease.Molecular neurobiology · 2026Review
- Preclinical evaluation of the CD38-targeting engineered toxin body MT-0169 against multiple myeloma.HemaSphere · 2024Article
- A review of the mechanisms of abnormal ceramide metabolism in type 2 diabetes mellitus, Alzheimer's disease, and their co-morbidities.Frontiers in pharmacology · 2024Review
- Potential Impact of Bioactive Compounds as NLRP3 Inflammasome Inhibitors: An Update.Current pharmaceutical biotechnology · 2024Review
- Shiga toxin 2 A-subunit induces mitochondrial damage, mitophagy and apoptosis via the interaction of Tom20 in Caco-2 cells.Heliyon · 2023Article
- Clostridium perfringens virulence factors are nonredundant activators of the NLRP3 inflammasome.EMBO reports · 2023Article
- Involvement of inflammasomes in tumor microenvironment and tumor therapies.Journal of hematology & oncology · 2023Review
- The mechanism and relevant mediators associated with neuronal apoptosis and potential therapeutic targets in subarachnoid hemorrhage.Neural regeneration research · 2023Review
- Pyroptosis: the dawn of a new era in endometrial cancer treatment.Frontiers in oncology · 2023Review
- Antimicrobial, immunological and biochemical effects of florfenicol and garlic (Allium sativum) on rabbits infected with Escherichia coli serotype O55: H7.Veterinary research communications · 2022Article
- Understanding the Link between Inflammasome and Apoptosis through the Response of THP-1 Cells against Drugs Using Droplet-Based Microfluidics.ACS omega · 2022Article
- Inhibition of O-GlcNAcylation protects from Shiga toxin-mediated cell injury and lethality in host.EMBO molecular medicine · 2022Article
- Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation.Oxidative medicine and cellular longevity · 2022Article
- Inflammasome Contribution to the Activation of Th1, Th2, and Th17 Immune Responses.Frontiers in microbiology · 2022Review
- Role of NLRP3 Inflammasome in Rheumatoid Arthritis.Frontiers in immunology · 2022Review
- Particle Safety Assessment in Additive Manufacturing: From Exposure Risks to Advanced Toxicology Testing.Frontiers in toxicology · 2022Review
- Review
- The P2X7 Receptor in Osteoarthritis.Frontiers in cell and developmental biology · 2021Review
- Shiga toxin suppresses noncanonical inflammasome responses to cytosolic LPS.Science immunology · 2020Article
- Molecular Biology ofToxins · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Shiga toxin (Stx)-mediated immune responses, including the production of the proinflammatory cytokines tumor necrosis-α (TNF-α) and interleukin-1β (IL-1β), may exacerbate vascular damage and accelerate lethality. However, the immune signaling pathway activated in response to Stx is not well understood. Here, we demonstrate that enzymatically active Stx, which leads to ribotoxic stress, triggers NLRP3 inflammasome-dependent caspase-1 activation and IL-1β secretion in differentiated macrophage-like THP-1 (D-THP-1) cells. The treatment of cells with a chemical inhibitor of glycosphingolipid biosynthesis, which suppresses the expression of the Stx receptor globotriaosylceramide and subsequent endocytosis of the toxin, substantially blocked activation of the NLRP3 inflammasome and processing of caspase-1 and IL-1β. Processing and release of both caspase-1 and IL-1β were significantly reduced or abolished in Stx-intoxicated D-THP-1 cells in which the expression of NLRP3 or ASC was stably knocked down. Furthermore, Stx mediated the activation of caspases involved in apoptosis in an NLRP3- or ASC-dependent manner. In Stx-intoxicated cells, the NLRP3 inflammasome triggered the activation of caspase-8/3, leading to the initiation of apoptosis, in addition to caspase-1-dependent pyroptotic cell death. Taken together, these results suggest that Stxs trigger the NLRP3 inflammasome pathway to release proinflammatory IL-1β as well as to promote apoptotic cell death.
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