Research Papers:

Diisononyl phthalate aggravates allergic dermatitis by activation of NF-kB

Jun Kang, Jing Song, Shiping Shen, Baizhan Li, Xu Yang and Mingqing Chen _

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Oncotarget. 2016; 7:85472-85482. https://doi.org/10.18632/oncotarget.13403

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Jun Kang1,*, Jing Song1,*, Shiping Shen1, Baizhan Li2, Xu Yang1, Mingqing Chen1

1Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan 430079, Hubei, China

2Key Laboratory of the Three Gorges Reservoir Region’s Eco-Environment, Ministry of Education, Chongqing University, Chongqing 400045, China

*These authors have contributed equally to this work

Correspondence to:

Mingqing Chen, email: [email protected]

Keywords: allergic dermatitis, diisononyl phthalate (DINP), NF-kB, oxidative stress, thymic stromal lymphopoietin (TSLP)

Received: July 04, 2016     Accepted: October 27, 2016     Published: November 16, 2016


Several epidemiological studies have suggested a possible link between exposure to Diisononyl phthalate (DINP) and the development of allergies. These findings remain controversial since there is insufficient scientific evidence to assess the ability of DINP to influence allergic immune responses. In addition, the mechanisms behind DINP-caused allergic diseases have not been fully elucidated. In this study, Balb/c mice were orally exposed to DINP for 3 weeks and were then sensitized with fluorescein isothiocyanate (FITC). We showed that oral exposure to DINP could aggravate allergic-dermatitis-like lesions, indicated by an increase in the number of mast cells, and in increased skin edema in FITC-induced contact hypersensitivity. This deterioration was concomitant with increased total serum immunoglobulin-E and Th2 cytokines. We determined the oxidative damage and the activation of nuclear factor-kb (NF-kB). The data demonstrated that DINP could promote oxidative damage and the activation of NF-kB in the skin. The expression of thymic stromal lymphopoietin and the activation of signal transducer and activator of transcriptions 3, 5 and 6 were enhanced concomitant with exacerbated allergic dermatitis effects and the activation of NF-kB induced by DINP. These effects were alleviated by pyrollidine dithiocarbamate, an inhibitor of NF-kB. The results suggest that oral exposure to DINP aggravated allergic contact dermatitis, which was positively regulated via NF-kB.

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