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Willenbockel, C. T.

Publications and source records attributed to Willenbockel, C. T..

2 recordsLinked to original sources

Bayesian Stacking of Quantitative Adverse Outcome Pathways Isolates Primary Drivers of Liver Steatosis

The quantification of adverse outcome pathways (qAOPs) involving multiple converging pathways remains a fundamental challenge in toxicology. This difficulty is worsened by small in vitro datasets with missing values and heteroscedasticity, which limit the estimation of non-linear response functions and the robust estimation of uncertainty. To overcome these limitations, we developed a framework for estimating a Bayesian qAOP Ensemble (Bayesian qAOPE) that combines heteroscedastic dose-response functions with continuous splines and linear models. By combining multiple converging non-linear pathways through Bayesian stacking, the most meaningful pathways are identified, and strongly correlated responses are naturally accounted for. Applying our approach to a hepatic steatosis dataset, we demonstrate by exact Bayesian leave-one-out cross-validation that our framework yields an exceptional predictive performance suitable for the derivation of a probabilistically weighted Benchmark Dose (BMD). Our framework is highly adaptable and provides a chemical-agnostic, mathematically founded blueprint for integrating multiple converging pathways in a Bayesian network.

pharmacology and toxicology↗

Systematic comparison of temporal transcriptional responses to hepatotoxicants in primary human hepatocytes (PHH) and HepaRG cells using concentration-response modelling of gene co-expression networks

Next generation risk assessment of chemicals revolves around the use of mechanistic information without animal experimentation. In this regard, toxicogenomics has proven to be a useful tool to elucidate the underlying mechanisms of adverse effects of xenobiotics. In the present study, two widely used human in vitro hepatocyte culture systems, namely primary human hepatocytes (PHH) and human hepatoma HepaRG cells, were exposed to liver toxicants known to induce liver cholestasis, steatosis or necrosis. Benchmark concentration-response modelling was applied to transcriptomics gene co-expression networks (modules) in order to derive benchmark concentrations (BMCs) and to gain mechanistic insight into the hepatotoxic effects. BMCs derived by concentration-response modelling of gene co-expression modules recapitulated concentration-response modelling of individual genes. Although PHH and HepaRG cells showed overlap in deregulated genes and modules by the liver toxicants, PHH demonstrated a higher responsiveness, based on the lower BMCs of co-regulated gene modules. Such BMCs can be used as transcriptomics point of departure (tPOD) for assessing module-associated cellular (stress) pathways/processes. This approach identified clear tPODs of around maximum systemic concentration (Cmax) levels for the tested drugs, while for cosmetics ingredients the BMCs were 10-100 fold higher than the estimated plasma concentrations. This approach could serve next generation risk assessment practice to identify early responsive modules at low BMCs, that could be linked to key events in liver adverse outcome pathways. In turn, this can assist in delineating potential hazards of new test chemicals using in vitro systems and used in a risk assessment when BMCs are paired with chemical exposure assessment.

pharmacology and toxicology↗