Weyl A, Vanscheidt W, Weiss J M, Peschen M, Schopf E, Simon J
Department of Dermatology, University of Freiburg, Germany.
J Am Acad Dermatol. 1996 Mar;34(3):418-23. doi: 10.1016/s0190-9622(96)90432-6.
Leukocyte binding to endothelial cells (ECs) is thought to contribute to the pathogenesis of leg ulcers caused by chronic venous insufficiency. In other systems, such binding is mediated by the interaction of adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule- (VCAM-1) and E-selectin (on ECs), and leukocyte function-associated antigen-1(LFA-1) and very late activated antigen-4 (VLA-4) (on Leukocytes).
Our purpose was to determine whether an increased expression of these adhesion molecules contributes to the pathogenesis of chronic venous insufficiency.
Twenty-seven biopsy specimens of inflamed dermatoliposclerotic skin adjacent to venous leg ulcers were stained immunohistochemically with monoclonal antibodies against ICAM-1, VCAM-1, LFA-1, VLA-4, and E-selectin. Staining intensity was compared with that of normal skin.
Specimens of leg ulcers caused by chronic venous insufficiency showed increased expression of ICAM-1 and VCAM-1 but not of E-selectin on The expression of LFA-1 and VLA-4 on perivascular leukocytes was increased dramatically in comparison to healthy skin.
Upregulation of ICAM-1 and VCAM-1 on ECs may contribute to the increased adherence and extravasation of LFA-1 and VLA-4-positive leukocytes in chronic venous insufficiency.
白细胞与内皮细胞（ECs）的结合被认为与慢性静脉功能不全所致腿部溃疡的发病机制有关。在其他系统中，这种结合是由细胞间黏附分子-1（ICAM-1）、血管细胞黏附分子-1（VCAM-1）和E-选择素（存在于ECs上）等黏附分子与白细胞功能相关抗原-1（LFA-1）和极晚期活化抗原-4（VLA-4）（存在于白细胞上）之间的相互作用介导的。
我们的目的是确定这些黏附分子表达的增加是否与慢性静脉功能不全的发病机制有关。
用抗ICAM-1、VCAM-1、LFA-1、VLA-4和E-选择素的单克隆抗体对27例腿部静脉溃疡旁炎性皮肤脂肪硬化的活检标本进行免疫组织化学染色。将染色强度与正常皮肤进行比较。
慢性静脉功能不全所致腿部溃疡标本显示ICAM-1和VCAM-1表达增加，但E-选择素表达未增加。与健康皮肤相比，血管周围白细胞上LFA-1和VLA-4的表达显著增加。
ECs上ICAM-1和VCAM-1的上调可能导致慢性静脉功能不全时LFA-1和VLA-4阳性白细胞的黏附和外渗增加。
