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031 Abnormal elevation of galactose aggravates inflammation and epidermal proliferation in psoriasis

      Psoriasis is an immune-mediated inflammatory skin disease which is associated with clinical features of metabolic syndrome. Galactose is a key source of energy and crucial structure element in complex molecules. Whether galactose is involved in psoriasis pathogenesis remains unclear. The aim of this study is to explore the association between galactose metabolism and psoriasis in human and the role that galactose plays in immiquimod (IMQ)-induced psoriasis mouse model. The levels of galactose, glucose and lipid metabolism index in fasting blood were compared between 30 healthy controls and 60 psoriasis vulgaris patients without diabetes or metabolic syndrome. The correlation between galactose and other metabolism index was analyzed. Galactose was gavage administrated into IMQ-induced psoriasis mice to test its influence on epidermal thickning, inflammatory cell infiltration and cytokines production. The effect of galactose on HaCaT cell proliferation was measured by the CCK-8 assay. We found that fasting blood galactose, insulin resistance and triglyceride were higher, while high density lipoprotein was lower significantly in psoriasis (p<0.05). Serum galactose level positively correlated with insulin resistance, triglyceride, while negatively correlated with apolipoprotein A in psoriasis (p<0.05). Excess galactose promoted psoriasis skin severity, ear swelling, epidermal thickning, CD45+ cell infiltration, the mRNA levels of inflammatory cytokine IL-1β, IL-6, IL-17F and IL-23 in IMQ-induced psoriasis lesions, and proliferation of HaCaT cells. In conclusion, Abnormal elevation of galactose in psoriasis vulgaris patients is associated with insulin resistance and lipid disorder. Excess galactose induced inflammation and epidermal proliferation in psoriasis model, indicating that galactose might promote the development of psoriasis.