ArticleJournal of immunology (Baltimore, Md. : 1950)2009
NLRP3 (NALP3, Cryopyrin) facilitates in vivo caspase-1 activation, necrosis, and HMGB1 release via inflammasome-dependent and -independent pathways.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
208 citing papers in PubMed, 347 citations in OpenAlex.
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- Emerging signal transduction pathways and the role of bacterial extracellular vesicles linked to the pathogenesis of endometriosis.Communications medicine · 2026Review
- Effect of alpha-lipoic acid and myoinositol on endometrial inflammation in women with unexplained recurrent pregnancy loss.Archives of gynecology and obstetrics · 2026Article
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- Function and mechanism of miRNAs during the process ofBiomolecules & biomedicine · 2025Review
- An anti-complement homogeneous polysaccharide fromActa pharmaceutica Sinica. B · 2025Article
- Insights into the roles of macrophages in Klebsiella pneumoniae infections: a comprehensive review.Cellular & molecular biology letters · 2025Review
- Caspase-11 and NLRP3 exacerbate systemic Klebsiella infection through reducing mitochondrial ROS production.Frontiers in immunology · 2025Article
- Role of the Receptor for Advanced Glycation End Products (RAGE) and Its Ligands in Inflammatory Responses.Biomolecules · 2024Review
- Modification macrophage to foam cells in atherosclerosis disease: some factors stimulate or inhibit this process.Journal of diabetes and metabolic disorders · 2024Review
- Mycobacterium intracellulare mediates macrophage pyroptosis by activating AIM2 and NLRP3 inflammasomes.Veterinary research communications · 2024Article
- Inhibitors of NLRP3 Inflammasome Formation: A Cardioprotective Role for the Gasotransmitters Carbon Monoxide, Nitric Oxide, and Hydrogen Sulphide in Acute Myocardial Infarction.International journal of molecular sciences · 2024Review
- GC/HRMS Analysis of E-Liquids Complements In Vivo Modeling Methods and can Help to Predict Toxicity.ACS omega · 2024Article
- Melatonin suppresses TLR4-mediated RSV infection in the central nervous cells by inhibiting NLRP3 inflammasome formation and autophagy.Journal of cellular and molecular medicine · 2024Article
- The discovery of NLRP3 and its function in cryopyrin-associated periodic syndromes and innate immunity.Immunological reviews · 2024Review
- Connecting the Dots: The Cerebral Lymphatic System as a Bridge Between the Central Nervous System and Peripheral System in Health and Disease.Aging and disease · 2024Review
- Review
- Global trends in research on endothelial cells and sepsis between 2002 and 2022: A systematic bibliometric analysis.Heliyon · 2024Review
148 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Bacterial infection elicits a range of beneficial as well as detrimental host inflammatory responses. Key among these responses are macrophage/monocyte necrosis, release of the proinflammatory factor high-mobility group box 1 protein (HMGB1), and induction of the cytokine IL-1. Although the control of IL-1beta has been well studied, processes that control macrophage cell death and HMGB1 release in animals are poorly understood. This study uses Klebsiella pneumonia as a model organism because it elicits all three responses in vivo. The regulation of these responses is studied in the context of the inflammasome components NLRP3 and ASC, which are important for caspase-1 activation and IL-1beta release. Using a pulmonary infection model that reflects human infection, we show that K. pneumonia-induced mouse macrophage necrosis, HMGB1, and IL-1beta release are dependent on NLRP3 and ASC. K. pneumoniae infection of mice lacking Nlrp3 results in decreased lung inflammation and reduced survival relative to control, indicating the overall protective role of this gene. Macrophage/monocyte necrosis and HMGB1 release are controlled independently of caspase-1, suggesting that the former two responses are separable from inflammasome-associated functions. These results provide critical in vivo validation that the physiologic role of NLRP3 and ASC is not limited to inflammasome formation.
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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.