OBJECTIVE: In this study, we investigated the impact of dietary docosahexaenoic (DHA) and arachidonic acid (AA) on development and severity of allergen-induced dermatitis. STUDY DESIGN: In sensitized mice, skin inflammation was induced by ovalbumin. Mice received either a diet containing 0.015% DHA, 0.029% AA or the combination of both. The severity of dermatitis was evaluated by using a clinical skin score (CSS), followed by immunohistologic and cytokine analysis. To unravel potential mechanisms, interleukin (IL)-4 or tumor necrosis factor α-stimulated keratinocytes from the cell line Kera-308 was cultured with different DHA/AA compositions and analyzed regarding proliferation and cytokine production. RESULTS: Dietary DHA/AA significantly improved the severity of allergen-induced dermatitis as the CSS was reduced by 36 ± 23% (p=0.005). Furthermore, reduced epidermal KI67 expression, increased number of forkhead box P3(+) cells, and elevated IL-10 expression were determined in skin lesions of dietary-treated mice. Correspondingly, in vitro DHA/AA-treated keratinocytes exhibited increased IL-10 expression and produced less thymic stromal lymphopoietin. CONCLUSION: Dietary DHA/AA supplementation leads to a significant amelioration of allergen-induced dermatitis. This was accompanied with the presence of increased regulatory T cells and IL-10 expression in lesional skin. Moreover, we identify keratinocytes, which play a crucial role in the regulation of skin inflammation, as important targets of DHA/AA supplementation. Future studies are needed to clarify whether DHA/AA acts directly or whether its biologic active metabolites are responsible for these findings. This may unravel novel therapeutical compounds for allergen-induced dermatitis.
OBJECTIVE: In this study, we investigated the impact of dietary docosahexaenoic (DHA) and arachidonic acid (AA) on development and severity of allergen-induced dermatitis. STUDY DESIGN: In sensitized mice, skin inflammation was induced by ovalbumin. Mice received either a diet containing 0.015% DHA, 0.029% AA or the combination of both. The severity of dermatitis was evaluated by using a clinical skin score (CSS), followed by immunohistologic and cytokine analysis. To unravel potential mechanisms, interleukin (IL)-4 or tumor necrosis factor α-stimulated keratinocytes from the cell line Kera-308 was cultured with different DHA/AA compositions and analyzed regarding proliferation and cytokine production. RESULTS: Dietary DHA/AA significantly improved the severity of allergen-induced dermatitis as the CSS was reduced by 36 ± 23% (p=0.005). Furthermore, reduced epidermal KI67 expression, increased number of forkhead box P3(+) cells, and elevated IL-10 expression were determined in skin lesions of dietary-treated mice. Correspondingly, in vitro DHA/AA-treated keratinocytes exhibited increased IL-10 expression and produced less thymic stromal lymphopoietin. CONCLUSION: Dietary DHA/AA supplementation leads to a significant amelioration of allergen-induced dermatitis. This was accompanied with the presence of increased regulatory T cells and IL-10 expression in lesional skin. Moreover, we identify keratinocytes, which play a crucial role in the regulation of skin inflammation, as important targets of DHA/AA supplementation. Future studies are needed to clarify whether DHA/AA acts directly or whether its biologic active metabolites are responsible for these findings. This may unravel novel therapeutical compounds for allergen-induced dermatitis.