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结节病患者血液单核细胞与肺泡巨噬细胞间黏附分子表达的超微结构研究

Ultrastructural study of expression of adhesion molecules between blood monocytes and alveolar macrophages from patients with pulmonary sarcoidosis.

作者信息

Thole A A, Rodrigues C A, Milward G, Porto L C, Carvalho L

机构信息

Department of Histology and Embryology, State University of Rio de Janeiro, Brazil.

出版信息

J Submicrosc Cytol Pathol. 2001 Oct;33(4):419-24.

PMID:11989775
Abstract

Pulmonary sarcoidosis is a chronic inflammatory disorder characterized by the presence of activated T cells and alveolar macrophages at sites of inflammation. These cells are recovered from bronchoalveolar lavage (BAL) from sarcoid patients in order to evaluate the expression of various markers on cell surfaces that should determine the diagnosis in sarcoidosis. In this work we compared the expression of VLA-4, VLA-5, Mac-1, ICAM-1 and VCAM- 1 adhesion molecules, at ultrastructural level, between blood monocytes and alveolar macrophages obtained from BAL, from patients with pulmonary sarcoidosis. Cells obtained from blood and BAL were fixed, embedded in LRWhite and then ultrathin sections were incubated with monoclonal antibodies against VLA-4, VLA-5, Mac-1, ICAM-1 and VCAM-1. The results showed a more evident labelling of all adhesion molecules on alveolar macrophages when compared to blood monocytes. The labelling was seen at cell surface, at cytoplasm and small vacuoles. The differences on adhesion molecule distributions from blood monocytes to alveolar macrophages suggest that changes in the expression of these molecules occur during pulmonary inflammatory response. Lymphocytes from BAL or blood had a weak label for these molecules.

摘要

肺结节病是一种慢性炎症性疾病,其特征是在炎症部位存在活化的T细胞和肺泡巨噬细胞。从结节病患者的支气管肺泡灌洗(BAL)中获取这些细胞,以评估细胞表面各种标志物的表达情况,这些标志物应能确定结节病的诊断。在这项研究中,我们在超微结构水平上比较了肺结节病患者BAL获取的肺泡巨噬细胞与血液单核细胞之间VLA-4、VLA-5、Mac-1、ICAM-1和VCAM-1黏附分子的表达。从血液和BAL获取的细胞经固定、包埋于LRWhite中,然后超薄切片与抗VLA-4、VLA-5、Mac-1、ICAM-1和VCAM-1的单克隆抗体孵育。结果显示,与血液单核细胞相比,肺泡巨噬细胞上所有黏附分子的标记更为明显。标记见于细胞表面、细胞质和小泡。从血液单核细胞到肺泡巨噬细胞黏附分子分布的差异表明,这些分子的表达变化发生在肺部炎症反应过程中。来自BAL或血液的淋巴细胞对这些分子的标记较弱。

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