title: Modulation of human dermal microvascular endothelial cells by Sarcoptes scabiei in combination with proinflammatory cytokines, histamine, and lipid-derived biologic mediators.
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.
authors.affiliation: Department of Pathology, Wright State University, Dayton, OH 45435, USA.
authors.forename: B Laurel
authors.initials: BL
authors.lastname: Elder
authors.forename: Larry G
authors.initials: LG
authors.lastname: Arlian
authors.forename: Marjorie S
authors.initials: MS
authors.lastname: Morgan
mesh_terms: D000818:Animals; D002457:Cell Extracts; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000378:metabolism; D016207:Cytokines / Q000494:pharmacology*; D020405:Dermis / Q000098:blood supply*; D042783:Endothelial Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000276:immunology*; D006632:Histamine / Q000494:pharmacology*; D006801:Humans; D018836:Inflammation Mediators / Q000494:pharmacology*; D007375:Interleukin-1 / Q000494:pharmacology; D015850:Interleukin-6 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D007975:Leukotriene B4 / Q000494:pharmacology; D008055:Lipids / Q000494:pharmacology; D055806:Microvessels / Q000166:cytology; D012520:Sarcoptes scabiei / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; D002457:Cell Extracts; D018932:Chemokine CCL2; D016207:Cytokines; D018836:Inflammation Mediators; D007375:Interleukin-1; D015850:Interleukin-6; D016209:Interleukin-8; D008055:Lipids; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D007975:Leukotriene B4; D006632:Histamine