US EPA

5532876 

Journal Article 

TRPA1 mediated aggravation of allergic contact dermatitis induced by DINP and regulated by NF-κB activation 

Kang, J; Ding, Y; Li, B; Liu, H; Yang, X; Chen, M 

2017 

1 

Scientific Reports
EISSN: 2045-2322 

NATURE PUBLISHING GROUP 

LONDON 

7 

43586 

English 

28240277 

10.1038/srep43586 

WOS:000394938100001 

http://www.nature.com/articles/srep43586
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The possible pathogenic role and mechanism of Di-iso-nonyl phthalate (DINP) in allergic dermatitis is still controversial. This work has shown that oral exposure to DINP exacerbated allergic dermatitis tissue lesions in FITC-sensitized mice. The lesions was accompanied by an enhancement of TRPA1 expression and an increase in IgG1, IL-6 and IL-13 levels. This work also found that blocking TRPA1 by HC030031 effectively prevented the development of allergic dermatitis resulting from oral exposure to DINP and/or FITC-sensitized mice. This result is marked by the down regulation of IgG1 levels, a reduction in mast cell degranulation and a decrease in IL-6 and IL-13 levels. We also showed that blocking NF-κB inhibited TRPA1 expression, and that blocking TRPA1 had no significant effect on the activation of NF-κB or TSLP expression. This study helps in understanding the role DINP exposure plays in the development of allergic dermatitis and provides new insight into the mechanisms behind the DINP-induced adjuvant effect. 

Acetanilides/pharmacology; Animals; Cell Degranulation/drug effects/immunology; Dermatitis, Allergic Contact/drug therapy/etiology/metabolism/pathology; Disease Models, Animal; Disease Progression; Gene Expression Regulation; Immunohistochemistry; Mast Cells/drug effects/immunology/metabolism