Staphylococcus epidermidis Activates Aryl Hydrocarbon Receptor Signaling in Human Keratinocytes: Implications for Cutaneous Defense
Staphylococcus epidermidis Activates Aryl Hydrocarbon Receptor Signaling in Human Keratinocytes: Implications for Cutaneous Defense
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DOI：
10.1159/000492162
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发表时间：
2019-01-01
影响因子：
5.3
通讯作者：
Harder, Juergen
中科院分区：
文献类型：
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作者：
Rademacher, Franziska;Simanski, Maren;Harder, Juergen
丰富的皮肤共生表皮葡萄球菌对角质形成细胞的细菌攻击会诱导独特的先天免疫反应，但潜在的分子机制仍在不断出现。我们报告说，在感染表皮葡萄球菌的人原代角质形成细胞中，芳基碳氢化合物受体（AhR）被激活，导致诱导AhR反应基因细胞色素P450 1A1（CYP1A1）。此外，表皮葡萄球菌介导的角质形成细胞中IL-β表达的诱导需要功能性AhR。 IL-β 和 CYP1A1 的 AhR 依赖性基因诱导由因子介导
Bacterial challenge of keratinocytes with the abundant skin commensal Staphylococcus epidermidis induces distinct innate immune responses, but the underlying molecular mechanisms are still emerging. We report that the aryl hydrocarbon receptor (AhR) was activated in human primary keratinocytes infected with S. epidermidis, leading to induction of the AhR-responsive gene cytochrome P450 1A1 (CYP1A1). In addition, functional AhR was required for S. epidermidis-mediated induction of IL-beta expression in keratinocytes. AhR-dependent gene induction of IL-beta and CYP1A1 was mediated by factor(s)