Increased expression of CD11b and functional changes in eosinophils after migration across endothelial cell monolayers.
Increased expression of CD11b and functional changes in eosinophils after migration across endothelial cell monolayers.
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跨内皮细胞单层迁移后，CD11b 表达增加，嗜酸性粒细胞功能发生变化。
DOI：
10.4049/jimmunol.150.9.4061
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发表时间：
1993
影响因子：
4.4
通讯作者：
P. Bruijnzeel
中科院分区：
文献类型：
--
作者：
C. Walker;S. Rihs;R. Braun;S. Betz;P. Bruijnzeel
与血液嗜酸性粒细胞相比，来自哮喘患者痰液、鼻息肉和支气管肺泡灌洗液的嗜酸性粒细胞显示 CD11b 表达显着增加。此外，组织嗜酸性粒细胞表达ICAM-1（CD54）和HLA-DR，而外周血嗜酸性粒细胞则不表达。体外外周血嗜酸性粒细胞跨过 IL-1 激活的人脐静脉内皮细胞单层的迁移导致 CD11b 和 CD35 表达显着上调，不诱导 ICAM-1 或 HLA-DR，并且 CD11a、CD29 和 CD32 表达小幅但显着降低。这些变化只能部分由未激活或 IL-1 激活的内皮细胞、血小板激活因子或各种重组细胞因子的上清液诱导。因此，由受体-配体结合或内皮细胞膜结合介质介导的细胞间相互作用，而不是可溶性因子，是造成嗜酸性粒细胞表面标志物表达改变的原因。事实上，IL-1 刺激的内皮细胞膜片段的制备能够诱导 CD11b 的上调，而血小板活化因子拮抗剂 WEB 2086 或抗 ELAM-1、VCAM-1 或 ICAM-1 的抗体无法抑制这种上调。对嗜酸性粒细胞上 CD11b 表达增加的功能意义的研究表明，粘附或迁移能力仅发生很小的变化。然而，CD11b 表达的增加与调理酵母聚糖刺激后产生超氧化物的能力增加有关。因此，嗜酸性粒细胞和内皮细胞之间的细胞间相互作用诱导嗜酸性粒细胞上 CD11b 和 CD35 的显着上调，并增加产生氧化爆发的能力。
Eosinophils from sputum, nasal polyps, and bronchoalveolar lavages of asthmatics demonstrated a considerably increased CD11b expression, compared with blood eosinophils. Furthermore, the tissue eosinophils expressed ICAM-1 (CD54) and HLA-DR, whereas peripheral blood eosinophils did not. In vitro migration of peripheral blood eosinophils across IL-1-activated human umbilical vein endothelial cell monolayers caused a considerable up-regulation of CD11b and CD35 expression, no induction of ICAM-1 or HLA-DR, and a small but significant decrease in CD11a, CD29, and CD32 expression. These changes were only partially inducible with supernatants from nonactivated or IL-1-activated endothelial cells, platelet-activating factor, or a variety of recombinant cytokines. Thus, cell-cell interactions mediated by receptor-ligand binding or endothelial cell membrane-bound mediators, rather than soluble factors, are responsible for the altered eosinophil surface marker expression. Indeed, preparations of membrane fragments from IL-1-stimulated endothelial cells were able to induce up-regulation of CD11b, which was not inhibitable with the platelet-activating factor antagonist WEB 2086 or antibodies against ELAM-1, VCAM-1, or ICAM-1. Investigation of the functional significance of the increased CD11b expression on eosinophils revealed only minimal changes in the adherence or transmigration capacity. Nevertheless, increased CD11b expression was related to an increased capacity to generate superoxide after stimulation with opsonized zymosan. Thus, cell-cell interactions between eosinophils and endothelial cells induce a considerable up-regulation of CD11b and CD35 on eosinophils and an increased capacity to generate an oxidative burst.