ArticleToxicology and applied pharmacology2014
Modeling toxicodynamic effects of trichloroethylene on liver in mouse model of autoimmune hepatitis.
Article in Toxicology and applied pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Immune effects of trichloroethylene: key findings of occupational hypersensitivity syndrome and its pathogenesis.Archives of toxicology · 2026Review
- Understanding Autoimmunity: Mechanisms, Predisposing Factors, and Cytokine Therapies.International journal of molecular sciences · 2024Review
- Developmental trichloroethylene exposure enhances predictive markers of autoimmunity in a sex-specific manner in disease-resistant female mice.Toxicology and applied pharmacology · 2022Article
- Differential Expression of miRNAs in Trichloroethene-Mediated Inflammatory/Autoimmune Response and Its Modulation by Sulforaphane: Delineating the Role of miRNA-21 and miRNA-690.Frontiers in immunology · 2022Article
- Gut microbiome-host interactions in driving environmental pollutant trichloroethene-mediated autoimmunity.Toxicology and applied pharmacology · 2021Article
- Redox-sensitive Nrf2 and MAPK signaling pathways contribute to trichloroethene-mediated autoimmune disease progression.Toxicology · 2021Article
- Aberrant Gut Microbiome Contributes to Intestinal Oxidative Stress, Barrier Dysfunction, Inflammation and Systemic Autoimmune Responses in MRL/lpr Mice.Frontiers in immunology · 2021Article
- Enhancing the Nrf2 Antioxidant Signaling Provides Protection Against Trichloroethene-mediated Inflammation and Autoimmune Response.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Sex-Dependent Effects on Liver Inflammation and Gut Microbial Dysbiosis After Continuous Developmental Exposure to Trichloroethylene in Autoimmune-Prone Mice.Frontiers in pharmacology · 2020Article
- Redox regulation of hepatic NLRP3 inflammasome activation and immune dysregulation in trichloroethene-mediated autoimmunity.Free radical biology & medicine · 2019Article
- Environmental Exposures and Autoimmune Diseases: Contribution of Gut Microbiome.Frontiers in immunology · 2019Review
- Opposing Actions of Developmental Trichloroethylene and High-Fat Diet Coexposure on Markers of Lipogenesis and Inflammation in Autoimmune-Prone Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Article
- A single dose of trichloroethylene given during development does not substantially alter markers of neuroinflammation in brains of adult mice.Journal of immunotoxicology · 2017Article
- Target Organ Metabolism, Toxicity, and Mechanisms of Trichloroethylene and Perchloroethylene: Key Similarities, Differences, and Data Gaps.The Journal of pharmacology and experimental therapeutics · 2016Review
- Environmental Basis of Autoimmunity.Clinical reviews in allergy & immunology · 2016Review
- Chronic exposure to water pollutant trichloroethylene increased epigenetic drift in CD4(+) T cells.Epigenomics · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Chronic exposure to industrial solvent and water pollutant trichloroethylene (TCE) in female MRL+/+mice generates disease similar to human autoimmune hepatitis. The current study was initiated to investigate why TCE-induced autoimmunity targeted the liver. Compared to other tissues the liver has an unusually robust capacity for repair and regeneration. This investigation examined both time-dependent and dose-dependent effects of TCE on hepatoprotective and pro-inflammatory events in liver and macrophages from female MRL+/+mice. After a 12-week exposure to TCE in drinking water a dose-dependent decrease in macrophage production of IL-6 at both the transcriptional and protein level was observed. A longitudinal study similarly showed that TCE inhibited macrophage IL-6 production. In terms of the liver, TCE had little effect on expression of pro-inflammatory genes (Tnfa, Saa2 or Cscl1) until the end of the 40-week exposure. Instead, TCE suppressed hepatic expression of genes involved in IL-6 signaling (Il6r, gp130, and Egr1). Linear regression analysis confirmed liver histopathology in the TCE-treated mice correlated with decreased expression of Il6r. A toxicodynamic model was developed to estimate the effects of TCE on IL-6 signaling and liver pathology under different levels of exposure and rates of repair. This study underlined the importance of longitudinal studies in mechanistic evaluations of immuntoxicants. It showed that later-occurring liver pathology caused by TCE was associated with early suppression of hepatoprotection rather than an increase in conventional pro-inflammatory events. This information was used to create a novel toxicodynamic model of IL-6-mediated TCE-induced liver inflammation.
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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.