Modulation of human dermal microvascular endothelial cells by Sarcoptes scabiei in combination with proinflammatory cytokines, histamine, and lipid-derived biologic mediators.

Department of Pathology, Wright State University, Dayton, OH 45435, USA.
Cytokine (Impact Factor: 2.87). 07/2009; 47(2):103-11. DOI: 10.1016/j.cyto.2009.05.008
Source: PubMed

ABSTRACT The ectoparasitic mite, Sarcoptes scabiei, produces molecules that depress initiation of host inflammatory and immune responses. Some of these down-regulate expression of adhesion molecules or secretion of chemokines or cytokines on and by cultured dermal endothelial cells (HMVEC-D). This study was undertaken to determine if the response of HMVEC-D to scabies is altered in the presence of various proinflammatory cytokines (tumor necrosis factor alpha and interleukins 1alpha, 1beta and 6), histamine, and lipid-derived mediators (prostaglandins D2 and E2, leukotriene B4, platelet activation factor) that likely occur in scabietic lesions in vivo. Scabies extract down-regulated the TNFalpha-induced expression of VCAM-1 by HMVEC-D and this down-regulation still occurred in the presence of the other proinflammatory cytokines, histamine or the lipid-derived mediators. Scabies inhibited the IL-1alpha and IL-1beta-induced secretion of IL-6, while a combination of scabies and histamine or LTB4 reduced the TNFalpha-induced secretion of IL-6. Scabies extract inhibited secretion of IL-8. Histamine, PGD2, PGE2, LTB4, PAF, and IL-6 alone had no effect on this inhibition, but the scabies-induced inhibition of IL-8 secretion was reduced in a dose-dependent fashion in the presence of IL-1alpha and IL-1beta.



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