ArticleLiver international : official journal of the International Association for the Study of the Liver2010
Acetaminophen-induced hepatic neutrophil accumulation and inflammatory liver injury in CD18-deficient mice.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 131 citations in OpenAlex.
- Platelets mediate neutrophil infiltration and exacerbate liver injury and sinusoidal endothelial cell damage after a severe acetaminophen overdose in mice.Archives of toxicology · 2025Article
- The effects of alpha-pinene against paracetamol-induced liver damage in male rats.Physiological reports · 2025Article
- Innate immune regulation in inflammation resolution and liver regeneration in drug-induced liver injury.Archives of toxicology · 2025Review
- Protective effects of Atractylodes macrocephala polysaccharides on acetaminophen-induced liver injury.Frontiers in pharmacology · 2025Article
- NLRP3 Inflammasome in Acute and Chronic Liver Diseases.International journal of molecular sciences · 2024Review
- The protective effect of Thai rice bran on N-acetyl-ρ-aminophen-induced hepatotoxicity in mice.Research in pharmaceutical sciences · 2024Article
- A liver digital twin for in silico testing of cellular and inter-cellular mechanisms in regeneration after drug-induced damage.iScience · 2024Article
- ERK/NF-kB/COX-2 Signaling Pathway Plays a Key Role in Curcumin Protection against Acetaminophen-Induced Liver Injury.Life (Basel, Switzerland) · 2023Article
- Analysis of AT7519 as a pro-resolution compound in an acetaminophen-induced mouse model of acute inflammation by UPLC-MS/MS.Journal of inflammation (London, England) · 2023Article
- Dose-dependent pleiotropic role of neutrophils during acetaminophen-induced liver injury in male and female mice.Archives of toxicology · 2023Article
- Cathelicidin promotes liver repair after acetaminophen-induced liver injury in mice.JHEP reports : innovation in hepatology · 2023Article
- Generation of pro-and anti-inflammatory mediators after acetaminophen overdose in surviving and non-surviving patients.Toxicology letters · 2022Article
- Review
- Molecular pathogenesis of acetaminophen-induced liver injury and its treatment options.Journal of Zhejiang University. Science. B · 2022Review
- Kupffer cells regulate liver recovery through induction of chemokine receptor CXCR2 on hepatocytes after acetaminophen overdose in mice.Archives of toxicology · 2022Article
- Neutrophil-Induced Liver Injury and Interactions Between Neutrophils and Liver Sinusoidal Endothelial Cells.Inflammation · 2021Review
- Two Faces of Neutrophils in Liver Disease Development and Progression.Hepatology (Baltimore, Md.) · 2021Review
- The complex roles of neutrophils in APAP-induced liver injury.Cell proliferation · 2021Review
- Late Protective Effect of Netrin-1 in the Murine Acetaminophen Hepatotoxicity Model.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- SPHK1 deficiency protects mice from acetaminophen-induced ER stress and mitochondrial permeability transition.Cell death and differentiation · 2020Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAcetaminophen (APAP) hepatotoxicity is currently the most frequent cause of acute liver failure in the US and many European countries. Although intracellular signalling mechanisms are critical for hepatocellular injury, a contribution of inflammatory cells, especially neutrophils, has been suggested. However, conflicting results were obtained when using immunological intervention strategies.
aimsThe role of neutrophils was investigated using a CD18-deficient mouse model.
resultsTreatment of C57Bl/6 wild type mice with 300 mg/kg APAP resulted in severe liver cell necrosis at 12 and 24 h. This injury was accompanied by formation of cytokines and chemokines and accumulation of neutrophils in the liver. However, there was no difference in the inflammatory response or liver injury in CD18-deficient mice compared with wild-type animals. In contrast to treatment with endotoxin, no upregulation of CD11b or priming for reactive oxygen was observed on neutrophils isolated from the peripheral blood or the liver after APAP administration. Furthermore, animals treated with endotoxin 3 h after APAP experienced an exaggerated inflammatory response as indicated by substantially higher cytokine and chemokine formation and twice the number of neutrophils in the liver. However, liver injury in the two-hit model was the same as with APAP alone.
conclusionsOur data do not support the hypothesis that neutrophils contribute to APAP hepatotoxicity or that a neutrophil-mediated injury phase could be provoked by a second, pro-inflammatory hit. Thus, APAP-induced liver injury in mice is dominated by intracellular mechanisms of cell death rather than by neutrophilic inflammation.
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