Expression of eosinophil-specific chemokines by human epithelial cells.
Expression of eosinophil-specific chemokines by human epithelial cells.
复制标题
人上皮细胞表达嗜酸性粒细胞特异性趋化因子。
DOI:
10.1159/000058785
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发表时间:
2000
影响因子:
--
通讯作者:
Beck,LA
中科院分区:
文献类型:
--
作者:
Stellato,C;Beck,LA
The preferential accumulation of eosinophils and/or deposition of eosinophil granule proteins in the tissues is one of the histological hallmarks of several inflammatory human diseases such as parasitic infestations and chronic allergic diseases. In chronic allergic asthma, a prototypic eosinophilic disease, it is now well established that eosinophils and their products, such as cytotoxic granule proteins and de novo synthesized leukotrienes, are involved in pathological changes seen in the airway mucosa, such as destruction of airway epithelium, sensitization of airway nerve terminals and vascular leakage [1–4]. The selective recruitment of eosinophils and other leukocytes within inflamed tissues is a complex, multistep process that involves leukocyte activation, margination, firm adhesion to endothelium and diapedesis [5]. Such process is likely mediated by the cooperative action of cytokines which cause eosinophil priming and increased survival (IL-3, IL-5, GM-CSF) with those which activate endothelium (IL-1, TNFa, IL-4, IL-13) and with eosinophil-selective chemoattractant molecules, especially chemokines [6]. Chemokines are a family of small, structurally related cytokines which include numerous potent eosinophil chemoattractants that are now thought to be important mediators of tissue eosinophilia. Although it is now apparent that the spectrum of activities of chemokines is broader than chemotaxis–including effects on angiogenesis, proliferation and apoptosis of a variety of cell types, participation in microbial pathogenesis–the regulation of leukocyte traffiking in both homeostatic and inflammatory states is unanimously recognized as a fundamental function of chemokines [7, 8]. The ‘classical’chemoattractants such as leukotriene B4, platelet-activating factor, C5a and N-formyl peptides display potent, but nonselective activity in recruiting inflammatory