ArticleJournal of immunology (Baltimore, Md. : 1950)2019
Computational Analysis Supports IL-17A as a Central Driver of Neutrophil Extracellular Trap-Mediated Injury in Liver Ischemia Reperfusion.
Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.
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.
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Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 citations in OpenAlex.
- Pooled it
- Interleukin-17 as a spatiotemporal bridge from acute to chronic inflammation: Novel insights from computational modeling.WIREs mechanisms of diseasePooled it
- The emerging role of neutrophil extracellular traps in liver diseases: a narrative review.Medical molecular morphology · 2026Review
- Review
- Neutrophil extracellular traps: A central player in liver diseases.Hepatology communications · 2026Review
- Dynamic regulation and targeted intervention of neutrophils in hepatic ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Peritoneal neutrophil extracellular traps contribute to septic AKI via peritoneal IL-17A and distant organ CXCL-1/ CXCL-2 pathway in abdominal sepsis.Scientific reports · 2026Article
- Neutrophil-T cell cross talk in noninfectious liver diseases.American journal of physiology. Gastrointestinal and liver physiology · 2026Review
- Mechanistic and functional characterization of NETs/IL-17 as a therapeutic target in EMT and brain metastasis of lung adenocarcinoma.Frontiers in immunology · 2026Article
- Research Trends in Neutrophil Extracellular Traps and Ischemia-Reperfusion Injury: A Dual-Database Bibliometric Analysis from 2013 to 2025.Journal of inflammation research · 2026Article
- Research progress on neutrophil extracellular traps and hepatitis-to-hepatocellular carcinoma transformation (Review).Oncology letters · 2026Review
- In Situ Assembly of Transformable Monopeptide on Activated Neutrophils Attenuates NETs-Induced Hepatocellular Carcinoma Metastasis by Disrupting NE Nuclear Translocation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neutrophil and macrophage zonation in liver disease: from spatiotemporal dynamics to advanced computational analysis.Frontiers in immunology · 2026Review
- Peritoneal Neutrophil Extracellular Traps contribute to septic AKI via peritoneal IL-17A and distant organ CXCL-1/ CXCL-2 pathway in abdominal sepsis.Research square · 2025Article
- Crosstalk between neutrophil extracellular traps and gut microbiota in ulcerative colitis: traditional Chinese medicine strategies.Frontiers in cellular and infection microbiology · 2025Review
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- Article
- Decoding Behcet's Uveitis: an In-depth review of pathogenesis and therapeutic advances.Journal of neuroinflammation · 2024Review
- Intertwined roles for GDF-15, HMGB1, and MIG/CXCL9 in Pediatric Acute Liver Failure.Frontiers in systems biology · 2024Article
- Transcriptome analysis revealed that ischemic post-conditioning suppressed the expression of inflammatory genes in lung ischemia-reperfusion injury.Frontiers in genetics · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Hepatic ischemia reperfusion (I/R) is a clinically relevant model of acute sterile inflammation leading to a reverberating, self-sustaining inflammatory response with resultant necrosis. We hypothesized that computerized dynamic network analysis (DyNA) of 20 inflammatory mediators could help dissect the sequence of post-I/R mediator interactions that induce injury. Although the majority of measured inflammatory mediators become elevated in the first 24 h, we predicted that only a few would be secreted early in the process and serve as organizational centers of downstream intermediator complexity. In support of this hypothesis, DyNA inferred a central organizing role for IL-17A during the first 3 h of reperfusion. After that, DyNA revealed connections among almost all the inflammatory mediators, representing an ongoing cytokine storm. Blocking IL-17A immediately after reperfusion disassembled the inflammatory networks and protected the liver from injury. Disassembly of the networks was not achieved if IL-17A blockage was delayed two or more hours postreperfusion. Network disassembly was accompanied by decrease in neutrophil infiltration and neutrophil extracellular trap (NET) formation. By contrast, administration of recombinant IL-17A increased neutrophil infiltration, NET formation, and liver necrosis. The administration of DNase, a NET inhibitor, significantly reduced hepatic damage despite prior administration of IL-17A, and DNase also disassembled the inflammatory networks. In vitro, IL-17A was a potent promoter of NET formation. Therefore, computational analysis identified IL-17A's early, central organizing role in the rapid evolution of a network of inflammatory mediators that induce neutrophil infiltration and NET formation responsible for hepatic damage after liver I/R.
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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.