title: [The vascular bed of the skin. Integration site of endogenous and exogenous stimuli].
abstract: Human skin is exposed to a great deal of environmental stimulation, which in predisposed individuals may cause specific inflammatory dermatosis. Typically, endothelial activation can be observed as the induced expression of cell adhesion molecules. This allows circulating immune cells to adhere to the endothelium and results in inflammatory, perivascular cell infiltrates in the affected tissue area. While tissue-derived cytokines have been discussed primarily as controlling factors of these inflammatory processes, recent evidence suggests direct endothelial activation by various exogenous impulses. Endothelial adhesion molecule expression has been found to be exclusively responsive to biochemical or biophysical stimulation, such as the concentration of metal ions, oxygen tension, UV radiation or mechanically operating shear stress without appreciable interaction of cytokines. These observations indicate that endothelial cells are capable of responding to exogenous stimulation, or rather transduce both exogenous and endogenous impulses, resulting in an integrative process. In view of this, individual deviations of endothelial cell functions need to be considered in pathophysiological concepts about diseases caused by external provocation, while their clinical relevance must be evaluated.
authors.affiliation: Dermatologische Klinik und Poliklinik, Ludwig-Maximillians-Universität, München.
authors.forename: M
authors.initials: M
authors.lastname: Heckmann
mesh_terms: D015815:Cell Adhesion Molecules / Q000502:physiology; D002450:Cell Communication / Q000502:physiology*; D003872:Dermatitis / Q000209:etiology / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D008833:Microcirculation / Q000503:physiopathology; D012867:Skin / Q000098:blood supply*
chemical_list: D015815:Cell Adhesion Molecules
vernacular_title: Das Gefässbett der Haut. Integrationsort endogener und exogener Reize.