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白细胞介素-4在特应性哮喘患者支气管黏膜嗜酸性粒细胞中的免疫定位

Immunolocalization of interleukin-4 in eosinophils in the bronchial mucosa of atopic asthmatics.

作者信息

Möller G M, de Jong T A, van der Kwast T H, Overbeek S E, Wierenga-Wolf A F, Thepen T, Hoogsteden H C

机构信息

Department of Pulmonary Diseases, Erasmus University, Rotterdam, The Netherlands.

出版信息

Am J Respir Cell Mol Biol. 1996 May;14(5):439-43. doi: 10.1165/ajrcmb.14.5.8624248.

DOI:10.1165/ajrcmb.14.5.8624248
PMID:8624248
Abstract

Several studies have shown that human eosinophils can synthesize and release a number of cytokines. The aim of this study was to investigate whether eosinophils contain interleukin (IL)-4 protein. We examined the ultrastructural localization of IL-4 in eosinophils in bronchial mucosal biopsies of 29 nonsmoking atopic asthmatics and 7 controls. No eosinophils were detected in the bronchial mucosa of controls. In the eosinophils (n = 42) of the asthmatics, IL-4 was localized to the electron-dense crystalloid core compartment of 85% of the secondary or specific eosinophil granules (n = 468). Other structures in the eosinophils were unlabeled. Control sections, incubated with an irrelevant primary antibody, were negative. This study demonstrates that pre-formed IL-4 is stored in the secondary eosinophil granules. These results were extended by light microscopic immunodouble-staining for IL-4 protein and eosinophil cationic protein, which showed that a subpopulation of activated eosinophils express IL-4 immunoreactivity in bronchial mucosal biopsies of asthmatics as well as controls. These data indicate that eosinophils may be an important source of IL-4 in allergic inflammation.

摘要

多项研究表明,人类嗜酸性粒细胞能够合成并释放多种细胞因子。本研究的目的是调查嗜酸性粒细胞是否含有白细胞介素(IL)-4蛋白。我们检测了29名不吸烟的特应性哮喘患者和7名对照者支气管黏膜活检组织中嗜酸性粒细胞内IL-4的超微结构定位。在对照者的支气管黏膜中未检测到嗜酸性粒细胞。在哮喘患者的嗜酸性粒细胞(n = 42)中,85%的次级或特异性嗜酸性粒细胞颗粒(n = 468)的电子致密晶体核心区域检测到IL-4。嗜酸性粒细胞中的其他结构未被标记。用无关一抗孵育的对照切片呈阴性。本研究表明,预先形成的IL-4储存于次级嗜酸性粒细胞颗粒中。通过对IL-4蛋白和嗜酸性粒细胞阳离子蛋白进行光镜免疫双染色扩展了这些结果,结果显示,在哮喘患者以及对照者的支气管黏膜活检组织中,活化嗜酸性粒细胞亚群表达IL-4免疫反应性。这些数据表明,嗜酸性粒细胞可能是变应性炎症中IL-4的重要来源。

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