Dexamethasone affects cytokine-mediated adhesion of HL-60 human promyelocytic leukemia cells to cultured dermal microvascular endothelial cells

Bibliographische Detailangaben
Veröffentlicht in:	Clinical immunology (Orlando, Fla.). - 1999. - 99(2001), 3 vom: 06. Juni, Seite 387-94
1. Verfasser:	Patel, N A (VerfasserIn)
Weitere Verfasser:	Patel, J A, Stins, M F, Kim, K S, Chang, S L
Format:	Aufsatz
Sprache:	English
Veröffentlicht:	2001
Zugriff auf das übergeordnete Werk:	Clinical immunology (Orlando, Fla.)
Schlagworte:	Journal Article Research Support, U.S. Gov't, P.H.S. E-Selectin Interleukin-1 Tumor Necrosis Factor-alpha Vascular Cell Adhesion Molecule-1 Intercellular Adhesion Molecule-1 126547-89-5 Dexamethasone 7S5I7G3JQL

Beschreibung
Zusammenfassung:	Copyright 2001 Academic Press. Leukocyte endothelial adhesion (LEA) is the prelude to a complex cascade of reactions following an immunological challenge. Recently, LEA has been implicated in the molecular basis of several dermatological disorders. While the role of proinflammatory cytokines, such as interleukin-1 beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha), in LEA has been investigated using nondermal models, limited data exist regarding their effects on LEA in dermal models. This study shows that cotreatment of cultured human dermal endothelial cells (CADMEC) with IL-1beta and TNF-alpha resulted in a marked increase in the adherence of human promyelocytic leukemia (HL-60) cells to CADMEC and an increase in expression of intercellular adhesion molecule-1 and E-selectin. Pretreatment of CADMEC with dexamethasone, a long-lasting glucocorticoid, resulted in a decrease in both HL-60 cell adhesion to CADMEC and adhesion molecule expression. Taken together, these data demonstrate that LEA may play a role in inflammatory skin conditions and in the mechanisms underlying the potential use of glucocorticoids as a treatment option
Beschreibung:	Date Completed 21.06.2001 Date Revised 21.11.2013 published: Print Citation Status MEDLINE
ISSN:	1521-6616