Abstract
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.
Highlights
Phthalates are widely used as plasticizers and can be found in PVC, toys, food packaging materials, medical bags and hoses, vinyl flooring, personal care products and hundreds of other products[1,2,3]
Di-iso-nonyl phthalate (DINP) exacerbated the expression of TRPA1 in an FITC-induced Allergic contact dermatitis (ACD) mouse model
To investigate the molecular mechanisms behind DINP exacerbated allergic dermatitis, we investigated the expression of TRPA1 in the skin of ears after the mice were exposed to DINP by oral gavage and sensitized with FITC
Summary
Phthalates are widely used as plasticizers and can be found in PVC, toys, food packaging materials, medical bags and hoses, vinyl flooring, personal care products and hundreds of other products[1,2,3]. Histamine receptors have been shown to stimulate sensory nerve fibers by activating a TRP ion channel subfamily V, member, 1 (TRPV1) in rodent models[20,21]. Another member of a TRP cation channel, subfamily A, member 1 (TRPA1), plays a dual role in conducting pain and itchiness[20]. The cytokine Thymic stromal lymphopoietin (TSLP) expressed mainly by epithelial cells, has been recognized as a key player in the pathogenesis of allergy diseases[25] It primes and stimulates DC maturation, and enhances the recruitment of Th2 effector cells[26]. Little is known about the relationship between a TRPA1 channel and the activation of NF-κB in CHS
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