ArticleJournal of neurochemistry2014
Critical role for the AIM2 inflammasome during acute CNS bacterial infection.
Article in Journal of neurochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 89 citations in OpenAlex.
- Article
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- AIM2 and IFI16 as nucleic acid sensors in Periodontitis-Driven systemic inflammation: emerging evidence and therapeutic implications.Clinical oral investigations · 2025Review
- Article
- Absent in Melanoma 2 Mediates Inflammasome Signaling Activation againstInternational journal of molecular sciences · 2024Article
- Strategies of bacterial detection by inflammasomes.Cell chemical biology · 2024Review
- The NLRP3 Inflammasome Is Dispensable in Methicillin-ResistantPathogens (Basel, Switzerland) · 2024Article
- Progress in understanding the role of cGAS-STING pathway associated with programmed cell death in intervertebral disc degeneration.Cell death discovery · 2023Review
- Intracellular bacteriolysis contributes to pathogenicity ofVirulence · 2022Article
- Essential Role of NLRP3 Inflammasome in Mediating IL-1β Production and the Pathobiology of Staphylococcus aureus Endophthalmitis.Infection and immunity · 2022Article
- Hyperkeratinization and Proinflammatory Cytokine Expression in Meibomian Glands Induced by Staphylococcus aureus.Investigative ophthalmology & visual science · 2021Article
- AIM2 controls microglial inflammation to prevent experimental autoimmune encephalomyelitis.The Journal of experimental medicine · 2021Article
- Activation and Immune Regulation Mechanisms of PYHIN Family During Microbial Infection.Frontiers in microbiology · 2021Review
- Immunopathogenesis of Craniotomy Infection and Niche-Specific Immune Responses to Biofilm.Frontiers in immunology · 2021Review
- Crosstalk between cGAS-STING signaling and cell death.Cell death and differentiation · 2020Review
- Review
- AIM2 in health and disease: Inflammasome and beyond.Immunological reviews · 2020Review
- TLR2 and caspase-1 signaling are critical for bacterial containment but not clearance during craniotomy-associated biofilm infection.Journal of neuroinflammation · 2020Article
- DNA Sensing in the Innate Immune Response.Physiology (Bethesda, Md.) · 2020Review
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin-1β (IL-1β) is essential for eliciting protective immunity during the acute phase of Staphylococcus aureus (S. aureus) infection in the central nervous system (CNS). We previously demonstrated that microglial IL-1β production in response to live S. aureus is mediated through the Nod-like receptor protein 3 (NLRP3) inflammasome, including the adapter protein ASC (apoptosis-associated speck-like protein containing a caspase-1 recruitment domain), and pro-caspase 1. Here, we utilized NLRP3, ASC, and caspase 1/11 knockout (KO) mice to demonstrate the functional significance of inflammasome activity during CNS S. aureus infection. ASC and caspase 1/11 KO animals were exquisitely sensitive, with approximately 50% of mice succumbing to infection within 24 h. Unexpectedly, the survival of NLRP3 KO mice was similar to wild-type animals, suggesting the involvement of an alternative upstream sensor, which was later identified as absent in melanoma 2 (AIM2) based on the similar disease patterns between AIM2 and ASC KO mice. Besides IL-1β, other key inflammatory mediators, including IL-6, CXCL1, CXCL10, and CCL2 were significantly reduced in the CNS of AIM2 and ASC KO mice, implicating autocrine/paracrine actions of IL-1β, as these mediators do not require inflammasome processing for secretion. These studies demonstrate a novel role for the AIM2 inflammasome as a critical molecular platform for regulating IL-1β release and survival during acute CNS S. aureus infection.
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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.