Mammalian skin protects our body against external assaults due to a well-organized skin barrier. The formation of the skin barrier is a complex process, in which basal keratinocytes lose their mitotic activity and differentiate to corneocytes. These corneocytes are embedded in intercellular lipid lamellae composed of ceramides, cholesterol, fatty acids, and cholesterol esters. Ceramides are the dominant lipid molecules and their reduction is connected with a transepidermal water loss and an epidermal barrier dysfunction resulting in inflammatory skin diseases. Moreover, bioactive sphingolipid metabolites like ceramide-1-phosphate, sphingosylphosphorylcholine, and sphingosine-1-phosphate are also involved in the biological modulation of keratinocytes and immune cells of the skin. Therefore, it is not astonishing that a dysregulation of sphingolipid metabolism has been identified in inflammatory skin diseases such as atopic dermatitis and psoriasis vulgaris. This chapter will describe not only the specific sphingolipid species and their skin functions but also the dysregulation of sphingolipid metabolism in inflammatory skin diseases.