Background:Staphylococcus aureus(S. aureus) is thought to play a significant role in the exacerbation of atopic dermatitis (AD). DS-Nh mice, a non-hair-bearing mouse model of AD, spontaneously develop dermatitis under conventional conditions. A remarkable increase in S. aureus is considered to strongly relate to the induction and aggravation of this dermatitis. A topical use of anatase-type titanium dioxide (TiO2) followed by UV irradiation, acting as photocatalyst, is believed to have antibacterial activity. We investigated the bactericidal effect of TiO2 with UV irradiation on DS-Nh mice to prevent the aggravation of the dermatitis. Methods: Ten-week-old DS-Nh mice were treated with TiO2 in petrolatum on the back, followed by UVA irradiation, for 11 weeks. The severity of dermatitis was assessed by evaluating individual lesions using a 4-grade scale and expressed as the total skin score. S. aureus colonizing the mouse skin was counted after isolation and incubation with agar medium. The skin barrier dysfunction was evaluated by measuring transepidermal water loss (TEWL). Results:The mice treated with TiO2 and UV irradiation showed a significant increase in total skin scores, the number of S. aureus and TEWL values, compared with non-treated mice. In contrast, these parameters were significantly lower in the mice treated with petrolatum and UV irradiation. Conclusions: A significant increase in S. aureus was recognized on the skin together with the aggravation of AD-like dermatitis in our mice model. Skin barrier dysfunction induced by TiO2 and UV irradiation seems to facilitate the increase in S. aureus.