ArticleToxicological sciences : an official journal of the Society of Toxicology2009
Coexposure of mice to trovafloxacin and lipopolysaccharide, a model of idiosyncratic hepatotoxicity, results in a unique gene expression profile and interferon gamma-dependent liver injury.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Evaluation of drug-induced liver toxicity of trovafloxacin and levofloxacin in a human microphysiological liver model.Scientific reports · 2023Article
- TDAG51 promotes transcription factor FoxO1 activity during LPS-induced inflammatory responses.The EMBO journal · 2023Article
- Tricyclic antidepressants induce liver inflammation by targeting NLRP3 inflammasome activation.Cell communication and signaling : CCS · 2023Article
- Icariside Ⅱ, a main compound in Epimedii Folium, induces idiosyncratic hepatotoxicity by enhancing NLRP3 inflammasome activation.Acta pharmaceutica Sinica. B · 2020Article
- What have we learned from animal models of idiosyncratic, drug-induced liver injury?Expert opinion on drug metabolism & toxicology · 2020Review
- Synergistic Cytotoxicity from Drugs and Cytokines In Vitro as an Approach to Classify Drugs According to Their Potential to Cause Idiosyncratic Hepatotoxicity: A Proof-of-Concept Study.The Journal of pharmacology and experimental therapeutics · 2017Article
- Calcium Contributes to the Cytotoxic Interaction Between Diclofenac and Cytokines.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Screening a mouse liver gene expression compendium identifies modulators of the aryl hydrocarbon receptor (AhR).Toxicology · 2015Article
- Cytotoxic Synergy Between Cytokines and NSAIDs Associated With Idiosyncratic Hepatotoxicity Is Driven by Mitogen-Activated Protein Kinases.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
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- Current challenges and controversies in drug-induced liver injury.Drug safety · 2012Article
- Comparison of TNFα to lipopolysaccharide as an inflammagen to characterize the idiosyncratic hepatotoxicity potential of drugs: Trovafloxacin as an example.International journal of molecular sciences · 2010Article
- Idiosyncratic drug-induced liver injury and the role of inflammatory stress with an emphasis on an animal model of trovafloxacin hepatotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2010Review
- Susceptibility to acetaminophen (APAP) toxicity unexpectedly is decreased during acute viral hepatitis in mice.Biochemical pharmacology · 2010Article
- Use of transcriptomics in understanding mechanisms of drug-induced toxicity.Pharmacogenomics · 2010Review
- Trovafloxacin enhances TNF-induced inflammatory stress and cell death signaling and reduces TNF clearance in a murine model of idiosyncratic hepatotoxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2009Article
- Trovafloxacin enhances the inflammatory response to a Gram-negative or a Gram-positive bacterial stimulus, resulting in neutrophil-dependent liver injury in mice.The Journal of pharmacology and experimental therapeutics · 2009Article
- Tumor necrosis factor alpha is a proximal mediator of synergistic hepatotoxicity from trovafloxacin/lipopolysaccharide coexposure.The Journal of pharmacology and experimental therapeutics · 2009Article
- Safety profile of the respiratory fluoroquinolone moxifloxacin: comparison with other fluoroquinolones and other antibacterial classes.Drug safety · 2009Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The antibiotic trovafloxacin (TVX) has caused severe idiosyncratic hepatotoxicity in people, whereas levofloxacin (LVX) has not. Mice cotreated with TVX and lipopolysaccharide (LPS), but not with LVX and LPS, develop severe hepatocellular necrosis. Mice were treated with TVX and/or LPS, and hepatic gene expression changes were measured before liver injury using gene array. Hepatic gene expression profiles from mice treated with TVX/LPS clustered differently from those treated with LPS or TVX alone. Several of the probe sets expressed differently in TVX/LPS-treated mice were involved in interferon (IFN) signaling and the janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway. A time course of plasma concentrations of IFN-gamma and interleukin (IL)-18, which directly induces IFN-gamma production, revealed that both cytokines were selectively increased in TVX/LPS-treated mice. Both IL-18(-/-) and IFN-gamma(-/-) mice were significantly protected from TVX/LPS-induced liver injury. In addition, IFN-gamma(-/-) mice had decreased plasma concentrations of tumor necrosis factor-alpha, IL-18, and IL-1beta when compared to wild-type mice. In conclusion, the altered expression of genes involved in IFN signaling in TVX/LPS-treated mice led to the finding that IL-18 and IFN-gamma play a critical role in TVX/LPS-induced liver injury.
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