ReviewCellular microbiology2020
Vying for the control of inflammasomes: The cytosolic frontier of enteric bacterial pathogen-host interactions.
Review in Cellular microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 26 citations in OpenAlex.
- GBP1 recruitment to actin-rich pedestals of extracellular Gram-negative bacteria promotes pyroptosis.The EMBO journal · 2026Article
- GBP1 recruitment to actin-rich pedestals induced by extracellular Gram negative bacteria promotes pyroptosis.bioRxiv : the preprint server for biology · 2025Article
- Review
- Genetic distribution, characterization, and function ofiScience · 2024Review
- Inflammasome activation by Gram-positive bacteria: Mechanisms of activation and regulation.Frontiers in immunology · 2023Review
- Caspase-11 interaction with NLRP3 potentiates the noncanonical activation of the NLRP3 inflammasome.Nature immunology · 2022Article
- Citrobacter rodentium(ϕStx2dact), a murine infection model for enterohemorrhagic Escherichia coli.Current opinion in microbiology · 2022Review
- A Probe for NLRP3 Inflammasome Inhibitor MCC950 Identifies Carbonic Anhydrase 2 as a Novel Target.ACS chemical biology · 2021Article
- Very long O-antigen chains of Salmonella Paratyphi A inhibit inflammasome activation and pyroptotic cell death.Cellular microbiology · 2021Article
- Clustering of Tir during enteropathogenic E. coli infection triggers calcium influx-dependent pyroptosis in intestinal epithelial cells.PLoS biology · 2020Article
- Yersinia pseudotuberculosis YopH targets SKAP2-dependent and independent signaling pathways to block neutrophil antimicrobial mechanisms during infection.PLoS pathogens · 2020Article
- Vying for the control of inflammasomes: The cytosolic frontier of enteric bacterial pathogen-host interactions.Cellular microbiology · 2020Review
- Lipopolysaccharide Recognition in the Crossroads of TLR4 and Caspase-4/11 Mediated Inflammatory Pathways.Frontiers in immunology · 2020Review
- From Welfare to Warfare: The Arbitration of Host-Microbiota Interplay by the Type VI Secretion System.Frontiers in cellular and infection microbiology · 2020Review
- The Radioprotective Effects of (-)-Epigallocatechin-3-gallate (EGCG): Restoring the Gut Microbiota-Immune Axis to Ameliorate Radiation-Induced Intestinal Injury.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Enteric pathogen-host interactions occur at multiple interfaces, including the intestinal epithelium and deeper organs of the immune system. Microbial ligands and activities are detected by host sensors that elicit a range of immune responses. Membrane-bound toll-like receptors and cytosolic inflammasome pathways are key signal transducers that trigger the production of pro-inflammatory molecules, such as cytokines and chemokines, and regulate cell death in response to infection. In recent years, the inflammasomes have emerged as a key frontier in the tussle between bacterial pathogens and the host. Inflammasomes are complexes that activate caspase-1 and are regulated by related caspases, such as caspase-11, -4, -5 and -8. Importantly, enteric bacterial pathogens can actively engage or evade inflammasome signalling systems. Extracellular, vacuolar and cytosolic bacteria have developed divergent strategies to subvert inflammasomes. While some pathogens take advantage of inflammasome activation (e.g. Listeria monocytogenes, Helicobacter pylori), others (e.g. E. coli, Salmonella, Shigella, Yersinia sp.) deploy a range of virulence factors, mainly type 3 secretion system effectors, that subvert or inhibit inflammasomes. In this review we focus on inflammasome pathways and their immune functions, and discuss how enteric bacterial pathogens interact with them. These studies have not only shed light on inflammasome-mediated immunity, but also the exciting area of mammalian cytosolic immune surveillance.
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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.