hc-030031 and Dermatitis--Allergic-Contact

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.

Topics: Acetanilides; Animals; Cell Degranulation; Dermatitis, Allergic Contact; Disease Models, Animal; Disease Progression; Gene Expression Regulation; Immunohistochemistry; Male; Mast Cells; Mice; NF-kappa B; Phthalic Acids; Purines; Signal Transduction; Th2 Cells; TRPA1 Cation Channel