ArticleCell reports2022
Neutrophil inflammasomes sense the subcellular delivery route of translocated bacterial effectors and toxins.
Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 22 citations in OpenAlex.
- TLR7/9 and type I interferon signaling reprogram neutrophil NET responses and impair antibacterial defense in systemic lupus erythematosus.Cell press blue · 2026Article
- A Biomimetic Copper-Caffeic Acid Nanozyme Activates Cuproptosis and Pyroptosis by Mimicking the Neutrophil Enzymatic Cascade.Advanced healthcare materials · 2026Article
- Threat assessment shapes neutrophil cell fate upon inflammasome activation.Science advances · 2026Article
- PANoptosis as a drug discovery framework: integrating cell death architecture with clinical translation.Genes and immunity · 2026Review
- Gasdermins against intracellular bacterial pathogens.Nature microbiology · 2026Review
- Convergent death programs in chronic obstructive pulmonary disease: how pyroptotic and ferroptotic crosstalk reshapes therapeutic paradigms.Frontiers in immunology · 2026Review
- Targeting inflammasome, IL-1β, and coagulation in melioidosis.Frontiers in microbiology · 2026Review
- How interactions between oxidized DNA and the NLRP3 inflammasome fuel inflammatory disease.Trends in biochemical sciences · 2025Review
- Live fast, die young: neutrophils streamline their metabolism to maximize inflammation.Infection and immunity · 2025Review
- ExoS effector in Pseudomonas aeruginosa Hyperactive Type III secretion system mutant promotes enhanced Plasma Membrane Rupture in Neutrophils.PLoS pathogens · 2025Article
- New insights into constitutive neutrophil death.Cell death discovery · 2025Review
- Inflammasome-mediated pyroptosis in defense against pathogenic bacteria.Immunological reviews · 2025Review
- Guards and decoys: RIPoptosome and inflammasome pathway regulators of bacterial effector-triggered immunity.PLoS pathogens · 2025Review
- NLRP1-dependent activation of Gasdermin D in neutrophils controls cutaneous leishmaniasis.PLoS pathogens · 2024Article
- Gasdermin E dictates inflammatory responses by controlling the mode of neutrophil death.Nature communications · 2024Article
- Type 3 secretion system induced leukotriene B4 synthesis by leukocytes is actively inhibited by Yersinia pestis to evade early immune recognition.PLoS pathogens · 2024Article
- NET formation is a default epigenetic program controlled by PAD4 in apoptotic neutrophils.Science advances · 2023Article
- Regulated cell death in neutrophils: From apoptosis to NETosis and pyroptosis.Seminars in immunology · 2023Review
- NLRP3 selectively drives IL-1β secretion by Pseudomonas aeruginosa infected neutrophils and regulates corneal disease severity.Nature communications · 2023Article
- Bucket lists must be completed during cell death.Trends in cell biology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
In neutrophils, caspase-11 cleaves gasdermin D (GSDMD), causing pyroptosis to clear cytosol-invasive bacteria. In contrast, caspase-1 also cleaves GSDMD but seems to not cause pyroptosis. Here, we show that this pyroptosis-resistant caspase-1 activation is specifically programmed by the site of translocation of the detected microbial virulence factors. We find that pyrin and NLRC4 agonists do not trigger pyroptosis in neutrophils when they access the cytosol from endosomal compartment. In contrast, when the same ligands penetrate through the plasma membrane, they cause pyroptosis. Consistently, pyrin detects extracellular Yersinia pseudotuberculosis ΔyopM in neutrophils, driving caspase-1-GSDMD pyroptosis. This pyroptotic response drives PAD4-dependent H3 citrullination and results in extrusion of neutrophil extracellular traps (NETs). Our data indicate that caspase-1, GSDMD, or PAD4 deficiency renders mice more susceptible to Y. pseudotuberculosis ΔyopM infection. Therefore, neutrophils induce pyroptosis in response to caspase-1-activating inflammasomes triggered by extracellular bacterial pathogens, but after they phagocytose pathogens, they are programmed to forego pyroptosis.
Indexed as
Identifiers
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.