Prediction of drug-induced liver injury using keratinocytes

被引:10
作者
Hirashima, Rika [1 ]
Itoh, Tomoo [1 ]
Tukey, Robert H. [2 ]
Fujiwara, Ryoichi [1 ]
机构
[1] Kitasato Univ, Sch Pharm, Minato Ku, 5-9-1 Shirokane, Tokyo 1088641, Japan
[2] Univ Calif San Diego, Dept Pharmacol, Lab Environm Toxicol, La Jolla, CA 92093 USA
关键词
keratinocyte; drug-induced liver injury; prediction; IL-1; beta; hepatotoxicity; EPIDERMAL NECROLYSIS; GENE-EXPRESSION; IMMUNE; INFLAMMATION; TOXICITY; FAILURE; MICE; HEPATOTOXICITY; ACTIVATION; NECROSIS;
D O I
10.1002/jat.3435
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Drug-induced liver injury (DILI) is one of the most common adverse drug reactions. DILI is often accompanied by skin reactions, including rash and pruritus. However, it is still unknown whether DILI-associated genes such as S100 calcium-binding protein A and interleukin (IL)-1 beta are involved in drug-induced skin toxicity. In the present study, most of the tested hepatotoxic drugs such as pioglitazone and diclofenac induced DILI-associated genes in human and mouse keratinocytes. Keratinocytes of mice at higher risk for DILI exhibited an increased IL-1 beta basal expression. They also showed a higher inducibility of IL-1 beta when treated by pioglitazone. Mice at higher risk for DILI showed even higher sums of DILI-associated gene basal expression levels and induction rates in keratinocytes. Our data suggest that DILI-associated genes might be involved in the onset and progression of drug-induced skin toxicity. Furthermore, we might be able to identify individuals at higher risk of developing DILI less invasively by examining gene expression patterns in keratinocytes. Copyright (C) 2017 John Wiley & Sons, Ltd.
引用
收藏
页码:863 / 872
页数:10
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