Xinran Xie1, Lei Zhang2, Yan Lin2, Yan Wang1, Weihong Liu2, Xue Li3, Ping Li4. 1. Beijing University of Chinese Medicine, Beijing, 100029, China; Beijing Institute of Traditional Chinese Medicine, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing Key Laboratory of Clinic and Basic Research with TCM on Psoriasis, Beijing, 100010, China. 2. Beijing Institute of Traditional Chinese Medicine, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing Key Laboratory of Clinic and Basic Research with TCM on Psoriasis, Beijing, 100010, China. 3. Beijing University of Chinese Medicine, Beijing, 100029, China. 4. Beijing Institute of Traditional Chinese Medicine, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing Key Laboratory of Clinic and Basic Research with TCM on Psoriasis, Beijing, 100010, China. Electronic address: liping411@126.com.
Abstract
BACKGROUND: Psoriasis patients are at increased risk of developing lipid metabolism disturbances. Both psoriasis and dyslipideamia not only closely interact in disease development, but occur as mutual side effects in some medicine treatment. The interactive mechanism of the two diseases is complicated and still unclear. OBJECTIVE: Here, we proposed applying imiquimod on the dorsal skin of ApoE-/- mice to establish a composite animal model which formed psoriasiform skin lesions under hyperlipidemic condition. METHOD: By comparison with corresponding wild-type(C57BL/6) mice, the composite mice model was evaluated by skin pathological features, lipid levels, immune inflammatory factors in order to clarify the diseases interplay mechanism. In addition, IL-17 mAb treatment was applied to observe the effect of IL-17 antibody on the composite animal model. RESULTS: The results verified that imiquimod-induced ApoE-/- mice model presented keratinocyte hyperplasia, parakeratosis, inflammatory cells infiltration and elevated serum lipid levels, and also reflected the complex interaction between inflammation and lipid metabolism. IL-17 mAb could inhibit psoriasis skin lesions with lipid accumulation via STAT3 pathway, but no influence on elevated serum cholesterol. CONCLUSIONS: Imiquimod-induced ApoE-/- mice model presented the pathological features of psoriasis and dyslipideamia, which could be an ideal composite animal model for the study of pathogenesis and pharmacotherapeutics of psoriasis and dyslipideamia comorbidity.
BACKGROUND:Psoriasispatients are at increased risk of developing lipid metabolism disturbances. Both psoriasis and dyslipideamia not only closely interact in disease development, but occur as mutual side effects in some medicine treatment. The interactive mechanism of the two diseases is complicated and still unclear. OBJECTIVE: Here, we proposed applying imiquimod on the dorsal skin of ApoE-/- mice to establish a composite animal model which formed psoriasiform skin lesions under hyperlipidemic condition. METHOD: By comparison with corresponding wild-type(C57BL/6) mice, the composite mice model was evaluated by skin pathological features, lipid levels, immune inflammatory factors in order to clarify the diseases interplay mechanism. In addition, IL-17 mAb treatment was applied to observe the effect of IL-17 antibody on the composite animal model. RESULTS: The results verified that imiquimod-induced ApoE-/- mice model presented keratinocyte hyperplasia, parakeratosis, inflammatory cells infiltration and elevated serum lipid levels, and also reflected the complex interaction between inflammation and lipid metabolism. IL-17 mAb could inhibit psoriasis skin lesions with lipid accumulation via STAT3 pathway, but no influence on elevated serum cholesterol. CONCLUSIONS:Imiquimod-induced ApoE-/- mice model presented the pathological features of psoriasis and dyslipideamia, which could be an ideal composite animal model for the study of pathogenesis and pharmacotherapeutics of psoriasis and dyslipideamia comorbidity.
Authors: Li-Hao Huang; Bernd H Zinselmeyer; Chih-Hao Chang; Brian T Saunders; Andrew Elvington; Osamu Baba; Thomas J Broekelmann; Lina Qi; Joseph S Rueve; Melody A Swartz; Brian S Kim; Robert P Mecham; Helge Wiig; Michael J Thomas; Mary G Sorci-Thomas; Gwendalyn J Randolph Journal: Cell Metab Date: 2018-11-08 Impact factor: 27.287