Prediction of drug-induced immune-mediated hepatotoxicity using hepatocyte-like cells derived from human embryonic stem cells

Toxicology. 2017 Jul 15:387:1-9. doi: 10.1016/j.tox.2017.06.005. Epub 2017 Jun 20.

Abstract

Drug-induced liver injury (DILI) is a leading cause of liver disease and a key safety factor during drug development. In addition to the initiation events of drug-specific hepatotoxicity, dysregulated immune responses have been proposed as major pathological events of DILI. Thus, there is a need for a reliable cell culture model with which to assess drug-induced immune reactions to predict hepatotoxicity for drug development. To this end, stem cell-derived hepatocytes have shown great potentials. Here we report that hepatocyte-like cells derived from human embryonic stem cells (hES-HLCs) can be used to evaluate drug-induced hepatotoxic immunological events. Treatment with acetaminophen significantly elevated the levels of inflammatory cytokines by hES-HLCs. Moreover, three human immune cell lines, Jurkat, THP-1, and NK92MI, were activated when cultured in conditioned medium obtained from acetaminophen-treated hES-HLCs. To further validate, we tested thiazolidinedione (TZD) class, antidiabetic drugs, including troglitazone withdrawn from the market because of severe idiosyncratic drug hepatotoxicity. We found that TZD drug treatment to hES-HLCs resulted in the production of pro-inflammatory cytokines and eventually associated immune cell activation. In summary, our study demonstrates for the first time the potential of hES-HLCs as an in vitro model system for assessment of drug-induced as well as immune-mediated hepatotoxicity.

Keywords: Drug-induced liver injury; Hepatocyte-kike cells derived from human embryonic stem cells; Human primary hepatocytes; Immune cells. drug screening system; Pro- and anti- inflammatory cytokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetaminophen / toxicity*
  • Analgesics, Non-Narcotic / toxicity*
  • Biological Assay*
  • Cell Differentiation*
  • Cell Survival / drug effects
  • Chemical and Drug Induced Liver Injury / etiology*
  • Chemical and Drug Induced Liver Injury / immunology
  • Chemical and Drug Induced Liver Injury / metabolism
  • Chemical and Drug Induced Liver Injury / pathology
  • Cytokines / immunology
  • Cytokines / metabolism
  • Embryonic Stem Cells / drug effects*
  • Embryonic Stem Cells / immunology
  • Embryonic Stem Cells / metabolism
  • Embryonic Stem Cells / pathology
  • Hepatocytes / drug effects*
  • Hepatocytes / immunology
  • Hepatocytes / metabolism
  • Hepatocytes / pathology
  • Humans
  • Hypoglycemic Agents / toxicity*
  • Inflammation Mediators / immunology
  • Inflammation Mediators / metabolism
  • Jurkat Cells
  • Phenotype
  • Risk Assessment
  • Thiazolidinediones / toxicity*
  • Toxicity Tests / methods*

Substances

  • Analgesics, Non-Narcotic
  • Cytokines
  • Hypoglycemic Agents
  • Inflammation Mediators
  • Thiazolidinediones
  • Acetaminophen