ArticleShock (Augusta, Ga.)2012
STAT1-deficient mice are resistant to cecal ligation and puncture-induced septic shock.
Article in Shock (Augusta, Ga.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- The Dual-Edged Sword: Risks and Benefits of JAK Inhibitors in Infections.Pathogens (Basel, Switzerland) · 2025Review
- Exploring the Anti-PANoptosis Mechanism of Dachaihu Decoction Against Sepsis-Induced Acute Lung Injury: Network Pharmacology, Bioinformatics, and Experimental Validation.Drug design, development and therapy · 2025Article
- CD5L as a promising biological therapeutic for treating sepsis.Nature communications · 2024Article
- Article
- High-dose ascorbic acid potentiates immune modulation through STAT1 phosphorylation inhibition and negative regulation of PD-L1 in experimental sepsis.Inflammopharmacology · 2024Article
- Modulation of Innate Immune Memory Dynamics by Subcellular Reactive Oxygen Species.Antioxidants & redox signaling · 2023Review
- Review
- Targeting HMGB1: An available Therapeutic Strategy for Breast Cancer Therapy.International journal of biological sciences · 2022Review
- New insights of necroptosis and immune infiltration in sepsis-induced myocardial dysfunction from bioinformatics analysis through RNA-seq in mice.Frontiers in cellular and infection microbiology · 2022Article
- Simultaneous C5 and CD14 inhibition limits inflammation and organ dysfunction in pig polytrauma.Frontiers in immunology · 2022Article
- The Study on the Regulation of Th Cells by Mesenchymal Stem Cells Through the JAK-STAT Signaling Pathway to Protect Naturally Aged Sepsis Model Rats.Frontiers in immunology · 2022Article
- The sepsis induced defective aggravation of immune cells: a translational science underling chemico-biological interactions from altered bioenergetics and/or cellular metabolism to organ dysfunction.Molecular and cellular biochemistry · 2021Review
- Development of Exhausted Memory Monocytes and Underlying Mechanisms.Frontiers in immunology · 2021Article
- TICAM2-related pathway mediates neutrophil exhaustion.Scientific reports · 2020Article
- Protective Effect of Epigallocatechin-3-Gallate (EGCG) in Diseases with Uncontrolled Immune Activation: Could Such a Scenario Be Helpful to Counteract COVID-19?International journal of molecular sciences · 2020Review
- Monophosphoryl lipid A prevents impairment of medullary thick ascending limb [Formula: see text] absorption and improves plasma [Formula: see text] concentration in septic mice.American journal of physiology. Renal physiology · 2018Article
- The biology of natural killer cells during sepsis.Immunology · 2018Review
- Rotavirus Degrades Multiple Interferon (IFN) Type Receptors To Inhibit IFN Signaling and Protects against Mortality from Endotoxin in Suckling Mice.Journal of virology · 2018Article
- Immunobiology of the IL-15/IL-15Rα complex as an antitumor and antiviral agent.Cytokine & growth factor reviews · 2017Review
- IL-15 Enables Septic Shock by Maintaining NK Cell Integrity and Function.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
STAT1 (signal transducer and activator of transcription 1) is a member of the JAK-STAT signaling family and plays a key role in facilitating gene transcription in response to activation of the types I and II interferon (IFN) receptors. TYK2 is essential for type I, but not type II, IFN-induced STAT1 activation. Previous studies show that STAT1-deficient mice are resistant to endotoxin-induced shock. The goal of the present study was to assess the response of STAT1- and TYK2-deficient mice to septic shock caused by cecal ligation and puncture (CLP). End points included survival, core temperature, organ injury, systemic cytokine production, and bacterial clearance. Results showed that survival rates were significantly higher in STAT1 knockout (STAT1KO) mice compared with wild-type controls (80% vs. 10%). The improved survival of STAT1KO mice was associated with less hypothermia, metabolic acidosis, hypoglycemia, and hepatocellular injury. Plasma interleukin 6, MIP-2, CXCL10, and IFN-α concentrations were significantly lower in STAT1KO mice than in wild-type mice. In the absence of antibiotic treatment, blood and lung bacterial counts were significantly lower in STAT1KO mice than in controls. However, treatment with antibiotics ablated that difference. A survival advantage was not observed in TYK2-deficient mice compared with control. However, CLP-induced hypothermia and systemic interleukin 6 and CXCL10 production were significantly attenuated in TYK2-deficient mice. These results indicate that STAT1 activation is an important factor in the pathogenesis of CLP-induced septic shock and is associated with the development of systemic inflammation and organ injury. TYK2 activation also appears to contribute to CLP-induced inflammation, but to a lesser extent than STAT1.
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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.