ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Activation of the NLRP3 inflammasome by group B streptococci.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
88 citing papers in PubMed, 147 citations in OpenAlex.
- Time to rethink prevention of neonatal group B streptococcal disease.Seminars in immunopathology · 2026Review
- Caspase-8 silences cell death-independent constitutive immune activation driven by tonic TNF-α.EMBO reports · 2026Article
- Cinnamaldehyde inhibits the NLRP3 inflammasome and inflammatory response by reducing oxidative stress in Neisseria gonorrhoeae-infected macrophages.Journal of traditional and complementary medicine · 2026Article
- Reduced NLRP3, AIM2 and NLRC4 inflammasome activity in cord blood of extremely preterm infants.Frontiers in pediatrics · 2026Article
- Not all Group BFrontiers in cellular and infection microbiology · 2026Article
- Radiation meets inflammation: NLRP3 inflammasome at the core of radiation-induced cardiac injury.Journal of translational medicine · 2025Review
- The NLRP3 inflammasome: a pivotal orchestrator of multisystem diseases-from molecular mechanisms to therapeutic innovation.Molecular biology reports · 2025Review
- A CRISPRi library screen in group BInfection and immunity · 2025Article
- Group B streptococcal infections in pregnancy and early life.Clinical microbiology reviews · 2025Review
- Group B Streptococcal Membrane Vesicles Induce Proinflammatory Cytokine Production and Are Sensed in an NLRP3 Inflammasome-Dependent Mechanism in a Human Macrophage-like Cell Line.ACS infectious diseases · 2025Article
- A CRISPRi Library Screen in Group BbioRxiv : the preprint server for biology · 2024Article
- Linking NLRP3 inflammasome and pulmonary fibrosis: mechanistic insights and promising therapeutic avenues.Inflammopharmacology · 2024Review
- Caspase-8 inhibition improves the outcome of bacterial infections in mice by promoting neutrophil activation.Cell reports. Medicine · 2023Article
- A detailed molecular network map and model of the NLRP3 inflammasome.Frontiers in immunology · 2023Review
- Macrophage polarization duringFrontiers in microbiology · 2023Article
- Dysregulated monocyte-derived macrophage response to Group BFrontiers in immunology · 2023Article
- Mechanisms of group BReproduction & fertility · 2022Review
- Neutrophils discriminate live from dead bacteria by integrating signals initiated by Fprs and TLRs.The EMBO journal · 2022Article
- Innate Immune Memory and the Host Response to Infection.Journal of immunology (Baltimore, Md. : 1950) · 2022Review
- Translating known drivers of COVID-19 disease severity to design better SARS-CoV-2 vaccines.Current opinion in virology · 2022Review
28 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
15 authors at 4 institutions in 4 countries.
Funding
Abstract
Group B Streptococcus (GBS) is a frequent agent of life-threatening sepsis and meningitis in neonates and adults with predisposing conditions. We tested the hypothesis that activation of the inflammasome, an inflammatory signaling complex, is involved in host defenses against this pathogen. We show in this study that murine bone marrow-derived conventional dendritic cells responded to GBS by secreting IL-1β and IL-18. IL-1β release required both pro-IL-1β transcription and caspase-1-dependent proteolytic cleavage of intracellular pro-IL-1β. Dendritic cells lacking the TLR adaptor MyD88, but not those lacking TLR2, were unable to produce pro-IL-1β mRNA in response to GBS. Pro-IL-1β cleavage and secretion of the mature IL-1β form depended on the NOD-like receptor family, pyrin domain containing 3 (NLRP3) sensor and the apoptosis-associated speck-like protein containing a caspase activation and recruitment domain adaptor. Moreover, activation of the NLRP3 inflammasome required GBS expression of β-hemolysin, an important virulence factor. We further found that mice lacking NLRP3, apoptosis-associated speck-like protein, or caspase-1 were considerably more susceptible to infection than wild-type mice. Our data link the production of a major virulence factor by GBS with the activation of a highly effective anti-GBS response triggered by the NLRP3 inflammasome.
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What OpenQuestion holds
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.