Abstract: Mo Junluan, Zhang Lijun, Zhou Jichang, Gong Chunmei, Xu Yuanfei, Yang Hui Molecular Biology Laboratory, Shenzhen Center for Chronic Disease Control, Shenzhen 518020, China Corresponding authors: Yang Hui, Email: yh2009cn@aliyun.com; Zhou Jichang, Email: jichangzhou@gmail.com 【Abstract】 Objective To evaluate the effect of micronutrient selenium on atopic dermatitis-like skin lesions in mice. Methods After 4-week feed with forages lacking selenium, 40 BALB/c mice were randomly and equally divided into 4 groups: selenium deficiency group fed with forages containing 0.01 mg/kg selenium for 4 weeks, normal selenium supplementation group fed with forages containing 0.25 mg/kg selenium for 4 weeks, excessive selenium supplementation group fed with forages containing 3.00 mg/kg selenium for 4 weeks, and control group fed with forages containing 0.25 mg/kg selenium for 4 weeks. Then, atopic dermatitis-like skin lesions were induced by dinitrochlorobenzene （DNCB） in the mice in sensitized groups, including the selenium deficiency group, normal selenium supplementation group and excessive selenium supplementation group. During sensitization, the severity of dermatitis in mice was monitored. Three weeks after the sensitization, the total plasma IgE level and inflammatory cell count in whole blood were measured. Skin tissues from the back of mice were subjected to histopathological examination and the selenium level was detected. Statistical analysis was carried out by one-way analysis of variance for comparisons of IgE levels and cell counts among different groups, as well as by Pearson correlation analysis and linear regression analysis for analyzing the correlation of various indices with the selenium level. Results Six days after the sensitization, the dermatitis severity scores were significantly higher in the sensitized groups than in the control group （On day 6, 8, 11, 13, 15 and 18 after the sensitization, F = 44.897, 76.622, 114.866, 33.352, 28.605 and 11.271 respectively, all P < 0.01）. On day 11 after the sensitization, the dermatitis severity score was significantly higher in the excessive selenium supplementation group than in the selenium deficiency group and normal selenium supplementation group （both P < 0.05）. Compared with the control group, obvious pathological changes of dermatitis were observed in the sensitized mice, but there was no significant difference in the number of inflammatory cells in skin lesions among the 3 sensitized groups （all P > 0.05）. The inflammatory cell count in whole blood and total plasma IgE level in the sensitized mice increased along with the increase of dietary selenium levels, and the excessive selenium supplementation group showed higher total plasma IgE level （［167.17 ± 8.49］ μg/L） compared with the selenium deficiency group （［124.78 ± 5.32］ μg/L, t = 3.919, P < 0.05）, normal selenium supplementation group （［132.61 ± 4.71］ μg/L, t = 3.222, P < 0.05） and control group （［109.13 ± 0.79］ μg/L, t = 6.485, P < 0.05）. The selenium level in the skin tissues of sensitized mice was positively linearly correlated with the total plasma IgE level （r = 0.579, P < 0.001）, whole-blood white blood cell count （r = 0.414, P < 0.05）, neutrophil count （r = 0.439, P < 0.05）, lymphocyte count （r = 0.417, P < 0.05）and eosinophil count （r = 0.505, P < 0.01）. Conclusion Different dietary selenium levels showed different effects on the severity of dermatitis in mice, and more severe dermatitis occurred in the excessive selenium supplementation group.

Key words: Dermatitis, atopic, Selenium, Disease models, animal, Inflammation, Immunoglobulin E