ArticleJournal of immunology (Baltimore, Md. : 1950)2022
Active Release of eCIRP via Gasdermin D Channels to Induce Inflammation in Sepsis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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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.
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Who cites it
29 citing papers in PubMed, 28 citations in OpenAlex.
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Role of DLL4 in Neutrophil Aging and Impaired Clearance in Sepsis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Gasdermin D Cleavage and Cytokine Release, Indicative of Pyroptotic Cell Death, Induced by Ophiobolin A in Breast Cancer Cell Lines.International journal of molecular sciences · 2026Article
- Gasdermin D-driven pyroptosis in sepsis: mechanisms, therapeutic strategies, and clinical translation.Frontiers in immunology · 2026Review
- Extracellular caspase-1: a critical inducer and a therapeutic target of lung injury in gut ischemia-reperfusion.Frontiers in immunology · 2026Article
- DLL4+ neutrophils promote Notch1-mediated endothelial PANoptosis to exacerbate acute lung injury in sepsis.The Journal of clinical investigation · 2025Article
- Gasdermins: multifunctional effectors of membrane permeabilization across cellular compartments.The FEBS journal · 2025Review
- Disulfiram as an anti-inflammatory agent: mechanisms, nano-delivery strategies, and applications in non-oncologic diseases.RSC advances · 2025Review
- Pyroptosis in sepsis-associated acute kidney injury: mechanisms and therapeutic perspectives.Critical care (London, England) · 2025Review
- Extracellular Cold-Inducible RNA-Binding Protein: Progress from Discovery to Present.International journal of molecular sciences · 2025Review
- Extracellular cold-inducible RNA-binding protein in CNS injury: molecular insights and therapeutic approaches.Journal of neuroinflammation · 2025Review
- B-1a cells scavenge NETs to attenuate sepsis.Journal of leukocyte biology · 2024Article
- Disulfiram Improves Fat Graft Retention by Modulating Macrophage Polarization With Inhibition of NLRP3 Inflammasome-Mediated Pyroptosis.Aesthetic surgery journal · 2024Article
- An engineered poly(A) tail attenuates gut ischemia/reperfusion-induced acute lung injury.Surgery · 2024Article
- DAMPs and radiation injury.Frontiers in immunology · 2024Review
- Extracellular CIRP promotes Kupffer cell inflammatory polarization in sepsis.Frontiers in immunology · 2024Article
- Salmonella spvC gene suppresses macrophage/neutrophil antibacterial defense mediated by gasdermin D.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- A Synthetic Poly(A) Tail Targeting Extracellular CIRP Inhibits Sepsis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Pyroptosis-induced inflammation and tissue damage.Seminars in immunology · 2023Review
- Antigen-presenting aged neutrophils induce CD4+ T cells to exacerbate inflammation in sepsis.The Journal of clinical investigation · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Extracellular cold-inducible RNA binding protein (eCIRP) is an inflammatory mediator that causes inflammation and tissue injury in sepsis. Gasdermin D (GSDMD) is a protein that, when cleaved, forms pores in the cell membrane, releasing intracellular contents into the extracellular milieu to exacerbate inflammation. We hypothesize that eCIRP is released actively from viable macrophages via GSDMD pores. We found that LPS induced eCIRP secretion from macrophages into the extracellular space. LPS significantly increased the expression of caspase-11 and cleavage of the GSDMD, as evidenced by increased N-terminal GSDMD expression in RAW 264.7 cells and mouse primary peritoneal macrophages. GSDMD inhibitor disulfiram decreased eCIRP release in vitro. Treatment with glycine to prevent pyroptosis-induced cell lysis did not significantly decrease eCIRP release from LPS-treated macrophages, indicating that eCIRP was actively released and was independent of pyroptosis. Downregulation of GSDMD gene expression by siRNA transfection suppressed eCIRP release in vitro after LPS stimulation. Moreover, GSDMD
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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.