3 Results
3.1 TRPA1 deficiency ameliorates skin inflammation and suppresses scratching behavior ina DNCB-induced AD mouse model
To investigate the significance of the TRPA1 in AD, repeated cutaneous allergen exposure with DNCB was used to induce the AD murine model as mentioned in Figure 1 . Following DNCB treatment, the lesion skin of ears and dorsal with edema, erythema, excoriation, and scarring were sequentially observed. Interestingly, the dermatitis score was significantly decreased in DNCB-treated TRPA1-/-mice compared to DNCB-treated WT mice (Figure 2A ). Furthermore, we found that a TRPA1-/- had a protective effect in suppressing DNCB-induced ear thickening (Figure 2B ).
Consequently, we investigated the effects of TRPA1 on the scratching behavior in the DNCB-induced AD mouse model. The DNCB-treated WT mice showed more frequent scratching behavior compared to DNCB-treated TRPA1-/- mice (Figure 2C ). Moreover, typical characteristics of AD histopathology, including marked epidermal hyperplasia and increased cellular were observed in DNCB-treated WT mice and DNCB-treated TRPA1 -/- mice, as confirmed by microscopic analysis of H&E stained sections of dorsal and ear lesion skin (Figure 2D-2E ). Yet, the thickening of the epidermis and the infiltration of inflammatory cells were significantly decreased in DNCB-treated TRPA1-/- mice than DNCB-treated WT mice (Figure 2F-2G ). These results suggested that TRPA1 deficiency not only alleviates pruritus, but also has an inflammatory protective role in AD.