ArticleScience (New York, N.Y.)2013
Noncanonical inflammasome activation by intracellular LPS independent of TLR4.
Article in Science (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 967 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
967 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,505 citations in OpenAlex.
- Research hotspots and future trends in sepsis-associated acute kidney injury: a bibliometric and visualization analysis.Frontiers in medicine · 2024Pooled it
- Glis1 regulates metabolic programming by promoting H3K18 lactylation to alleviate neuronal senescence following spinal cord injury.Genes & diseases · 2027Article
- Subverting colonization resistance:Virulence · 2026Review
- Protocol for high-throughput identification of genes involved in pyroptotic cell death by live microscopy.STAR protocols · 2026Article
- A Novel Biofilm Amyloid Ligand for Caspase-11 Drives Hyperactivation in Dendritic Cells.bioRxiv : the preprint server for biology · 2026Article
- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- Article
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Innate immune sensors of inflammasomes and PANoptosomes: structural-mechanistic insights and therapeutic implications.Cell research · 2026Review
- When folding CARDs wins the game: molecular snapshots of lipopolysaccharide sensing by the non-canonical inflammasome.Biochemical Society transactions · 2026Review
- Pyroptosis in Patients with Ovarian Dysfunction and Infertility: Molecular Mechanisms and Therapeutics.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Structural insights into ligand-induced CARD assembly in inflammatory caspases.Research square · 2026Article
- Article
- IFN-α and IFN-β inhibit NLRP1-driven PANoptosis.EMBO reports · 2026Article
- RNF213-dependent lytic destruction ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Unanchored ubiquitin chains promote the non-canonical inflammasome via UBXN1.Research square · 2026Article
- Beyond Acute Infection: A Conceptual Framework Linking Zoonotic Bacterial Pathogens to Pulmonary Fibrosis and Lung Carcinogenesis.Biomedicines · 2026Review
- Gasdermin-Mediated Pyroptosis: Novel Strategies Against Colorectal Cancer.Cancer science · 2026Review
- Gut microbiota-atrium axis: Microbiota metabolite-mediated regulation of the NLRP3 inflammasome in atrial fibrillation-pathophysiological roles and therapeutic perspectives.Heart rhythm O2 · 2026Review
- Pyroptosis: Molecular mechanisms and function.Journal of physiology and biochemistry · 2026Review
907 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gram-negative bacteria including Escherichia coli, Citrobacter rodentium, Salmonella typhimurium, and Shigella flexneri are sensed in an ill-defined manner by an intracellular inflammasome complex that activates caspase-11. We show that macrophages loaded with synthetic lipid A, E. coli lipopolysaccharide (LPS), or S. typhimurium LPS activate caspase-11 independently of the LPS receptor Toll-like receptor 4 (TLR4). Consistent with lipid A triggering the noncanonical inflammasome, LPS containing a divergent lipid A structure antagonized caspase-11 activation in response to E. coli LPS or Gram-negative bacteria. Moreover, LPS-mutant E. coli failed to activate caspase-11. Tlr4(-/-) mice primed with TLR3 agonist polyinosinic:polycytidylic acid [poly(I:C)] to induce pro-caspase-11 expression were as susceptible as wild-type mice were to sepsis induced by E. coli LPS. These data unveil a TLR4-independent mechanism for innate immune recognition of LPS.
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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.