Extracts of Sarcoptes scabiei De Geer Downmodulate Secretion of IL-8 by Skin Keratinocytes and Fibroblasts and of GM-CSF by Fibroblasts in the Presence of Proinflammatory Cytokines

Previous in vitro studies showed that molecules in an extract of the mite Sarcoples scabiei variety canis De Geer could modulate the secretion of cytokines front cultured cultural normal human epidermal keratinocytes and dermal fibroblasts in the absence of proinflammatory cytokines in the cell culture media. The purpose of this study was to investigate whether scabies extract could also Modulate cytokine and chemokine secretion front epidermal keratinocytes and dermal fibroblasts in the presence of proinflammatory cytokines that are likely present in the scabietic lesion in vivo. In particular, could the downmodulating properties of this ectoparasitic mite oil Skin cells be maintained in the presence of proinflammatory cytokines? We found that even in the presence of the, proinflammatory cytokines interleukin (IL)-1 alpha, IL-1 beta, and a mixture of tumor necrosis factor (TNF)alpha + IL-17, scabies extract still downregulated the levels of IL-8 secretion from keratinocytes and fibroblasts and of granulocyte/macrophage-colony stimulating factor (GM-CSF) secretion front fibroblasts that were induced by stimulation of the cells with proinflammatory cytokines alone. This study also showed that scabies molecules induced secretions of growth-related oncogene a (GRO alpha), transforming growth factor alpha (TGF alpha), and cutaneous T-cell attracting chemokine (CTACK) from keratinocytes and IL-6 and granulocyte-colony stimulating factor (G-CSF) from fibroblasts. These findings, coupled with the previous findings that molecules in scabies extract could downregulate expression of intracellular adhesion molecule-1 (ICAM-1) and E-selectin by normal dermal microvascular endothelial cells and secretion of IL-1 ra from keratinocytes, suggest that multiple factors from scabies mites play a role in the characteristic delayed inflammatory response to a primary infestation with S. scabiei. These are adaptations that favor invasion of the host by the parasite.