ArticleProceedings of the National Academy of Sciences of the United States of America2016
NLRP3 inflammasome plays a redundant role with caspase 8 to promote IL-1β-mediated osteomyelitis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
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Who cites it
101 citing papers in PubMed, 128 citations in OpenAlex.
- Interleukin-1 Beta Gene Polymorphism rs16944 May Associate with Increased Susceptibility to Extremity Chronic Osteomyelitis in Chinese Han Population.BioMed research international · 2019Trial
- Review
- PANoptosis in life and death across cell types: From innate immunity to therapeutic implications.Cell chemical biology · 2026Review
- HSPCs and TScience advances · 2026Article
- Context-dependent roles of the NLRP3 inflammasome in osteomyelitis and strategies for precision modulation.Frontiers in immunology · 2026Review
- The role of PANoptosis in diabetes and its complications: mechanisms and therapeutic prospects.Frontiers in immunology · 2026Review
- Innate immune and metabolic signals induce mitochondria-dependent membrane lysis via mitoxyperiosis.Cell · 2025Article
- Role of PANoptosis in cancer: Molecular mechanisms and therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2025Review
- PTGS2 Silencing Inhibits Ferroptosis in Staphylococcus Aureus-induced Osteomyelitis By Blocking the IL-17A Signaling Pathway.Inflammation · 2025Article
- Three decades of caspases and RIPKs in life and death.Human molecular genetics · 2025Review
- Manipulating the PANoptosome: baseless hype or a newfound hope for human immunity?Apoptosis : an international journal on programmed cell death · 2025Review
- Disruption of Morrbid alleviates autoinflammatory osteomyelitis in Pstpip2-deficient mice.Disease models & mechanisms · 2025Article
- Innate immune sensor NLRP3 drives PANoptosome formation and PANoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Caspases: structural and molecular mechanisms and functions in cell death, innate immunity, and disease.Cell discovery · 2025Review
- Evolutionary and Functional Analysis of Caspase-8 and ASC Interactions to Drive Lytic Cell Death, PANoptosis.Molecular biology and evolution · 2025Article
- VX-765 alleviates motor and cognitive impairments via inhibiting PANoptosis activation in the neonatal rats after hypoxic-ischemic brain damage.Pediatric discovery · 2025Article
- Exploring the critical role of PANoptosis in the pathogenesis of intervertebral disc degeneration: mechanisms and potential therapeutic targets.Frontiers in cell and developmental biology · 2025Review
- Caspase-8 in inflammatory diseases: a potential therapeutic target.Cellular & molecular biology letters · 2024Review
- Inflammasomes at the Foundation of Inflammatory Cell Death Complexes.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- NLRC5 senses NADCell · 2024Article
41 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Missense mutation in the proline-serine-threonine phosphatase-interacting protein 2 (Pstpip2) gene results in the development of spontaneous chronic bone disease characterized by bone deformity and inflammation that is reminiscent of patients with chronic multifocal osteomyelitis (cmo). Interestingly, this disease is specifically mediated by IL-1β but not IL-1α. The precise molecular pathways that promote pathogenic IL-1β production inPstpip2(cmo)mice remain unidentified. Furthermore, how IL-1β provokes inflammatory bone disease inPstpip2(cmo)mice is not known. Here, we demonstrate that double deficiency of Nod like receptor family, pyrin domain containing 3 (NLRP3) and caspase 8 inPstpip2(cmo)mice provides similar protection as observed in caspase-1 and caspase-8-deficientPstpip2(cmo)mice, demonstrating redundant roles for the NLRP3 inflammasome and caspase 8 in provoking osteomyelitic disease inPstpip2(cmo)mice. Consistently, immunofluorescence studies exhibited distinct caspase-1 and caspase-8 puncta in diseasedPtpn6(spin)neutrophils. Data from our chimera studies demonstrated that IL-1β produced by hematopoietic cells is sensed by the radioresistant compartment to promote bone disease. Furthermore, our results showed that the IL-1β signaling is unidirectional and feedback signaling of IL-1β onto the hematopoietic compartment is not important for disease induction. In conclusion, our studies have uncovered the combined actions of the NLRP3 inflammasome and caspase 8 leading to IL-1β maturation and the directionality of IL-1β in driving disease inPstpip2(cmo)mice.
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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.