[ODP-216] Effects of emedastine and josamycin on atopic dermatitis like-skin lesions in NC/Nga mice
Objective: In this study, we evaluated the effect of topical application of Th1/Th2 inhibitors, emedastine and josamycin, on atopic dermatitis (AD).
Methods: The effects of anti-allergy drugs on TIM-4 expression in Langerhans cells (LCs) were examined to predict whether they would inhibit Th2 cell development. Next, mice were primed with ovalbumin (OVA)-pulsed LCs that had been treated with selected anti-allergy drugs. The cytokine response in the lymph nodes was investigated by ELISA. The therapeutic effects of emedastine and josamycin on AD were assessed using AD-like skin lesions of NC/Nga mice.
Results: As expected, OVA-pulsed LCs that had been treated with emedastine and injected into the footpads of mice inhibited Th2 cell development. Next, the therapeutic effects of emedastine and josamycin on AD were compared. Topical application of emedastine significantly suppressed the increase in the skin severity score in NC/Nga mice with AD-like skin lesions. This suppressive effect was associated with a decrease in the production of IFN-γ and IL-4 in auricular lymph node cells. However, its efficacy was not as marked as that of josamycin.
Conclusion: These results suggest that topical application of emedastine to skin lesions of AD patients, in some cases in combination with josamycin, may provide clinical benefits through the inhibition of Th1/Th2 cell development mediated by LCs.
Methods: The effects of anti-allergy drugs on TIM-4 expression in Langerhans cells (LCs) were examined to predict whether they would inhibit Th2 cell development. Next, mice were primed with ovalbumin (OVA)-pulsed LCs that had been treated with selected anti-allergy drugs. The cytokine response in the lymph nodes was investigated by ELISA. The therapeutic effects of emedastine and josamycin on AD were assessed using AD-like skin lesions of NC/Nga mice.
Results: As expected, OVA-pulsed LCs that had been treated with emedastine and injected into the footpads of mice inhibited Th2 cell development. Next, the therapeutic effects of emedastine and josamycin on AD were compared. Topical application of emedastine significantly suppressed the increase in the skin severity score in NC/Nga mice with AD-like skin lesions. This suppressive effect was associated with a decrease in the production of IFN-γ and IL-4 in auricular lymph node cells. However, its efficacy was not as marked as that of josamycin.
Conclusion: These results suggest that topical application of emedastine to skin lesions of AD patients, in some cases in combination with josamycin, may provide clinical benefits through the inhibition of Th1/Th2 cell development mediated by LCs.