ArticleScientific reports2015
Application of IL-36 receptor antagonist weakens CCL20 expression and impairs recovery in the late phase of murine acetaminophen-induced liver injury.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Immunobiological Properties and Clinical Applications of Interleukin-38 for Immune-Mediated Disorders: A Systematic Review Study.International journal of molecular sciences · 2021Pooled it
- The role of the interleukin family in liver fibrosis.Frontiers in immunology · 2025Review
- Saturated Fat-Mediated Upregulation of IL-32 and CCL20 in Hepatocytes Contributes to Higher Expression of These Fibrosis-Driving Molecules in MASLD.International journal of molecular sciences · 2023Article
- Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice.Frontiers in immunology · 2023Article
- Therapeutic Perspectives of IL1 Family Members in Liver Diseases: An Update.Journal of clinical and translational hepatology · 2022Review
- The immunological mechanisms and therapeutic potential in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.Cell & bioscience · 2022Review
- The Protective Role of IL-36/IL-36R Signal in Con A-Induced Acute Hepatitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- 3'mRNA sequencing reveals pro-regenerative properties of c5ar1 during resolution of murine acetaminophen-induced liver injury.NPJ Regenerative medicine · 2022Article
- Identification of Genes Regulating Hepatocyte Injury by a Genome-Wide CRISPR-Cas9 Screen.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Immunopathobiology and therapeutic targets related to cytokines in liver diseases.Cellular & molecular immunology · 2021Review
- The Role of IL-36 in Infectious Diseases: Potential Target for COVID-19?Frontiers in immunology · 2021Review
- LR12 Promotes Liver Repair by Improving the Resolution of Inflammation and Liver Regeneration in Mice with Thioacetamide- (TAA-) Induced Acute Liver Failure.Mediators of inflammation · 2021Article
- Protective effect of interleukin-36 receptor antagonist on liver injury induced by concanavalin A in mice.Iranian journal of basic medical sciences · 2020Article
- IL-36 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020Review
- Identification of Novel Regulatory Genes in APAP Induced Hepatocyte Toxicity by a Genome-Wide CRISPR-Cas9 Screen.Scientific reports · 2019Article
- Interleukin-36 in Infectious and Inflammatory Skin Diseases.Frontiers in immunology · 2019Review
- Interleukin-1 Family Cytokines: Keystones in Liver Inflammatory Diseases.Frontiers in immunology · 2019Review
- A Prominent Role of Interleukin-18 in Acetaminophen-Induced Liver Injury Advocates Its Blockage for Therapy of Hepatic Necroinflammation.Frontiers in immunology · 2018Article
- Article
- Type I Interferon Supports Inducible Nitric Oxide Synthase in Murine Hepatoma Cells and Hepatocytes and during Experimental Acetaminophen-Induced Liver Damage.Frontiers in immunology · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overdosing of the analgesic acetaminophen (APAP, paracetamol) is a major cause of acute liver injury. Whereas toxicity is initiated by hepatocyte necrosis, course of disease is regulated by mechanisms of innate immunity having the potential to serve in complex manner pathogenic or pro-regenerative functions. Interleukin (IL)-36γ has been identified as novel IL-1-like cytokine produced by and targeting epithelial (-like) tissues. Herein, we investigated IL-36γ in acute liver disease focusing on murine APAP-induced hepatotoxicity. Enhanced expression of hepatic IL-36γ and its prime downstream chemokine target CCL20 was detected upon liver injury. CCL20 expression coincided with the later regeneration phase of intoxication. Primary murine hepatocytes and human Huh7 hepatocellular carcinoma cells indeed displayed enhanced IL-36γ expression when exposed to inflammatory cytokines. Administration of IL-36 receptor antagonist (IL-36Ra) decreased hepatic CCL20 in APAP-treated mice. Unexpectedly, IL-36Ra likewise increased late phase hepatic injury as detected by augmented serum alanine aminotransferase activity and histological necrosis which suggests disturbed tissue recovery upon IL-36 blockage. Finally, we demonstrate induction of IL-36γ in inflamed livers of endotoxemic mice. Observations presented introduce IL-36γ as novel parameter in acute liver injury which may contribute to the decision between unleashed tissue damage and initiation of liver regeneration during late APAP toxicity.
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