Henseleit U, Steinbrink K, Sunderkötter C, Goebeler M, Roth J, Sorg C
Institute of Experimental Dermatology, University of Münster, Germany.
Exp Dermatol. 1995 Oct;4(5):249-56.
VCAM-1 (vascular cell adhesion molecule-1) is a cytokine-inducible adhesion molecule which is known to mediate adhesion of mononuclear cells to endothelial cells in vitro via binding to the integrin VLA-4 (very late antigen-4). To further elucidate the role and regulation of VCAM-1 in vitro, we compared in vitro and in vivo expression of VCAM-1 in response to cytokines and investigated immunohistochemically the expression of VCAM-1 in three murine models of experimental inflammation. These models differed with regard to the pathogenetic mechanism, and the subsesquent infiltrate: allergic contact dermatitis (ACD) to DNFB as a T cell-controlled, DTH type of inflammation, cutaneous infection with Leishmania major as a chronic granulomatous inflammation and the cauterized cornea as a model for acute inflammation. VCAM-1 was found to be markedly enhanced on vascular endothelia in all types of inflammation and after subcutaneous administration of LPS and TNF-alpha. Administration of IL-4, however, failed to induce VCAM-1 both in vivo and in vitro. The increased VCAM-1 expression in the inflammatory models correlated with the appearance of infiltrating monocytes/macrophages. A concomitant influx of CD4-positive/CD8-positive lymphocytes was only observed in ACD and Leishmaniasis.
血管细胞黏附分子-1（VCAM-1）是一种细胞因子诱导的黏附分子，已知其在体外通过与整合素VLA-4（极迟抗原-4）结合介导单核细胞与内皮细胞的黏附。为了进一步阐明VCAM-1在体外的作用和调节机制，我们比较了VCAM-1在体外和体内对细胞因子的反应表达，并通过免疫组织化学方法研究了VCAM-1在三种实验性炎症小鼠模型中的表达。这些模型在发病机制和随后的浸润情况方面有所不同：对二硝基氟苯（DNFB）的过敏性接触性皮炎（ACD）作为一种T细胞控制的迟发型超敏反应（DTH）类型的炎症，感染硕大利什曼原虫的皮肤作为慢性肉芽肿性炎症，以及烧灼角膜作为急性炎症模型。在所有类型的炎症中以及皮下注射脂多糖（LPS）和肿瘤坏死因子-α（TNF-α）后，发现血管内皮上的VCAM-1明显增强。然而，白细胞介素-4（IL-4）的给药在体内和体外均未能诱导VCAM-1。炎症模型中VCAM-1表达的增加与浸润的单核细胞/巨噬细胞的出现相关。仅在ACD和利什曼病中观察到CD4阳性/CD8阳性淋巴细胞的伴随流入。
