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小鼠血管细胞黏附分子-1在体外及体内不同炎症模型中的表达:与单核细胞迁移的相关性

Expression of murine VCAM-1 in vitro and in different models of inflammation in vivo: correlation with immigration of monocytes.

作者信息

Henseleit U, Steinbrink K, Sunderkötter C, Goebeler M, Roth J, Sorg C

机构信息

Institute of Experimental Dermatology, University of Münster, Germany.

出版信息

Exp Dermatol. 1994 Dec;3(6):249-56.

PMID:7538407
Abstract

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 vivo, 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 subsequent 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.

摘要

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,已知它在体外通过与整合素VLA-4(极晚期抗原-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在体内的作用和调控机制,我们比较了VCAM-1在体外和体内对细胞因子的反应性表达,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情况。这些模型在发病机制和随后的浸润情况方面存在差异:对二硝基氟苯(DNFB)的过敏性接触性皮炎(ACD),属于T细胞控制的迟发型超敏反应(DTH)型炎症;用硕大利什曼原虫进行皮肤感染,属于慢性肉芽肿性炎症;烧灼角膜作为急性炎症模型。结果发现,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,血管内皮上的VCAM-1均显著增强。然而,白细胞介素-4(IL-4)无论是在体内还是体外均未能诱导VCAM-1的表达。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性流入。

相似文献

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Expression of murine VCAM-1 in vitro and in different models of inflammation in vivo: correlation with immigration of monocytes.小鼠血管细胞黏附分子-1在体外及体内不同炎症模型中的表达:与单核细胞迁移的相关性
Exp Dermatol. 1994 Dec;3(6):249-56.
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Expression of murine VCAM-1 in vitro and in different models of inflammation in vivo: correlation with immigration of monocytes.小鼠血管细胞黏附分子-1在体外及体内不同炎症模型中的表达:与单核细胞迁移的相关性
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Hypoxia-induced mitogenic factor promotes vascular adhesion molecule-1 expression via the PI-3K/Akt-NF-kappaB signaling pathway.缺氧诱导有丝分裂因子通过PI-3K/Akt-NF-κB信号通路促进血管黏附分子-1的表达。
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Effects of lipopolysaccharide on endothelial cell adhesion molecule expression in interleukin-10 deficient mice.
脂多糖对白细胞介素-10缺陷小鼠内皮细胞黏附分子表达的影响。
Inflammation. 1999 Apr;23(2):99-110. doi: 10.1023/a:1020232826906.
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Anti-inflammatory drugs and endothelial cell adhesion molecule expression in murine vascular beds.抗炎药物与小鼠血管床中内皮细胞黏附分子的表达
Gut. 1999 Feb;44(2):186-95. doi: 10.1136/gut.44.2.186.