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.