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However, the exact mechanism by which <jats:styled-content style=\"fixed-case\">VOC<\/jats:styled-content>s induce an inflammatory response in the skin is poorly understood. Thymic stromal lymphopoietin (<jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content>) is known to be an important factor in the initiation and maintenance of allergic inflammatory diseases, including <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objectives<\/jats:title><jats:p>The aim of this work is to define the correlation between <jats:styled-content style=\"fixed-case\">VOC<\/jats:styled-content>s and <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>The present study demonstrates dose\u2010dependent increases of TSLP protein and <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> levels in keratinocytes following exposure to chloroform. We further investigated the regulatory mechanisms of chloroform\u2010induced TSLP expression in human keratinocytes.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Chloroform induces early growth response\u20101 (Egr\u20101) protein expression in human keratinocytes. This process is mediated by the c\u2010<jats:styled-content style=\"fixed-case\">JUN<\/jats:styled-content> N\u2010terminal kinase (<jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content>) and extracellular signal\u2010regulated kinase (<jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content>) signaling pathways. Inhibition of phosphorylated <jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content> significantly downregulated Egr\u20101 expression, which was subsequently associated with reduced <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content> expression in chloroform\u2010exposed human keratinocytes. Moreover, treatment of Egr\u20101 si<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> abolished chloroform\u2010induced <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content> protein expression and <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content> promoter transcriptional activation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Taken together, these findings suggest that, in human keratinocytes, the upregulation of <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content> by chloroform is induced through an Egr\u20101\u2010dependent mechanism that requires the c\u2010<jats:styled-content style=\"fixed-case\">JNK<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">ERK<\/jats:styled-content> pathways. Our results suggest that exposure to chloroform may aggravate allergic skin diseases such as <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content> through Egr\u20101\u2010dependent <jats:styled-content style=\"fixed-case\">TSLP<\/jats:styled-content> regulation.<\/jats:p><\/jats:sec>","DOI":"10.1111\/ijd.12946","type":"journal-article","created":{"date-parts":[[2015,10,17]],"date-time":"2015-10-17T02:29:22Z","timestamp":1445048962000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Chloroform upregulates early growth response\u20101\u2010dependent thymic stromal lymphopoietin expression via the <scp>JNK<\/scp> and ERK pathways in human keratinocytes"],"prefix":"10.1111","volume":"54","author":[{"given":"Hana","family":"Lee","sequence":"first","affiliation":[{"name":"Laboratory of Cell Signaling and Nanomedicine Department of Dermatology Korea University College of Medicine Seoul South 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