ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014
Interleukin-4 deficiency protects mice from acetaminophen-induced liver injury and inflammation by prevention of glutathione depletion.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Good Cells Go Bad: Immune Dysregulation in the Transition from Acute Liver Injury to Liver Failure After Acetaminophen Overdose.Drug metabolism and disposition: the biological fate of chemicals · 2024Review
- The immunological mechanisms and therapeutic potential in drug-induced liver injury: lessons learned from acetaminophen hepatotoxicity.Cell & bioscience · 2022Review
- Review
- Mitochondrial depolarization and repolarization in the early stages of acetaminophen hepatotoxicity in mice.Toxicology · 2020Article
- IL-33 signalling in liver immune cells enhances drug-induced liver injury and inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- The impact of sterile inflammation in acute liver injury.Journal of clinical and translational research · 2017Article
- Imaging liver biology in vivo using conventional confocal microscopy.Nature protocols · 2015Article
- Assessing the Effect of Leptin on Liver Damage in Case of Hepatic Injury Associated with Paracetamol Poisoning.Gastroenterology research and practice · 2015Article
- Cannabidiol rescues acute hepatic toxicity and seizure induced by cocaine.Mediators of inflammation · 2015Article
- Drug-induced hepatotoxicity: metabolic, genetic and immunological basis.International journal of molecular sciences · 2014Review
- Interleukin-4 and acetaminophen hepatotoxicity: a story of conflicting results and conclusions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2014Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInterleukin-4 (IL-4) is a multifunctional cytokine involved in many diseases such as autoimmune hepatitis and idiosyncratic drug reactions. However, its role in acetaminophen (APAP)-induced liver injury remains unclear. Our objective was to evaluate the contribution of IL-4 to the pathogenesis of APAP-induced liver injury.
methodsBalb/C (WT) and IL-4 knockout (IL-4(-/-)) mice were orally overdosed with APAP. After 24 h, survival percentage, biochemical and morphological markers of liver injury, and tissue inflammation were assessed.
resultsIL-4(-/-) mice were protected from APAP toxicity. Intravital confocal microscopy, tissue histology and serum ALT levels showed significantly less liver injury and inflammation than in the WT group, which may explain the increased survival rate of IL-4(-/-) mice. In addition, IL-4(-/-) mice had decreased production of tumor necrosis factor α, CXCL1 and interleukin-1β in the liver, but not in a remote site such as the lungs. Hepatic macrophage activation was markedly reduced in IL-4-deficient mice. In addition, glutathione depletion-a primary cause of APAP-mediated injury-was significantly attenuated in IL-4(-/-) mice.
conclusionsTaken together, our data demonstrate that IL-4(-/-) mice are protected from APAP-induced liver injury due to reduced depletion of glutathione, which prevented liver damage and tissue inflammation.
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