In patients with
atopic dermatitis, alcoholic beverages can sometimes trigger or enhance
itching. We have previously reported that HR-1 hairless mice fed a commercial special diet, HR-AD, but not a normal diet, develop
atopic dermatitis-like skin
inflammation with prolonged spontaneous scratching, and that skin barrier dysfunction is involved in the basal scratching. In the present study, the effects of
ethanol on itch-related scratching were examined in this mouse model. When
ethanol (30%, 10 ml/kg) was given orally to HR-AD-fed mice, scratching with long duration was further markedly increased, while oral
ethanol administration had little effect on the scratching response in normal diet-fed mice. The scratching response after oral
ethanol administration in HR-AD-fed mice (
ethanol-induced scratching) was attenuated by antagonism of the
mu-opioid receptor or local skin
anesthesia, as in human
itching.
Ethanol-induced scratching was also suppressed by improvement of skin barrier function by an application of
petrolatum ointment, while
ethanol administration itself did not affect the function. This suggests that
ethanol indirectly aggravates the basal scratching. Although antagonism of the transient receptor potential vanilloid-1 did not affect
ethanol-induced scratching, blockade of
ethanol actions in the central nervous system (CNS), including
gamma-aminobutyric acid type A receptor antagonism and
N-methyl-d-aspartate receptor activation, inhibited it. Taken together, the present study demonstrates that orally administered
ethanol markedly aggravates itch-related scratching in HR-AD-fed mice developing
atopic dermatitis, and suggests that the CNS depressant actions of
ethanol play an important role in the aggravation.