REGULATION OF TRANSENDOTHELIAL NEUTROPHIL MIGRATION BY ENDOGENOUS INTERLEUKIN-8

REGULATION OF TRANSENDOTHELIAL NEUTROPHIL MIGRATION BY ENDOGENOUS INTERLEUKIN-8
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DOI:
10.1126/science.1718038
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发表时间:
1991-10-04
期刊:
影响因子:
56.9
通讯作者:
WEISS, SJ
WEISS, SJ
中科院分区:
综合性期刊1区
文献类型:
--
作者:
HUBER, AR;KUNKEL, SL;WEISS, SJ

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中性粒细胞从血流到发炎组织的运动取决于中性粒细胞和内皮细胞的激活。 毛细血管后微静脉的内皮细胞通过表达粘附分子和合成多种趋化因子对促炎介质作出反应。 内皮细胞产生的白细胞介素-8(IL-8)的77个氨基酸的变体被认为是中性粒细胞通过血管壁模型侵入的必要条件。 由细胞因子或脂多糖刺激的内皮细胞分泌的IL-8诱导中性粒细胞凝集素粘附分子-1的快速脱落、白细胞β-2整合素的上调以及中性粒细胞的附着和迁移。 因此,内源性内皮IL-8调节急性炎症反应期间的经小静脉运输。
Movement of neutrophils from the bloodstream to inflamed tissue depends on the activation of both the neutrophil and the endothelial cell. Endothelial cells lining the postcapillary venule respond to proinflammatory mediators by expressing adhesion molecules and synthesizing a variety of neutrophil-activating factors. Endothelial cell production of a 77-amino acid variant of interleukin-8 (IL-8) was found to be a requirement for the invasion of neutrophils through a vessel wall model. IL-8 secreted by cytokine- or lipopolysaccharide-stimulated endothelial cells induced the rapid shedding of neutrophil lectin adhesion molecule-1, the up-regulation of leukocyte beta-2 integrins, and the attachment and transmigration of the neutrophils. Thus, endogenous endothelial IL-8 regulates transvenular traffic during acute inflammatory responses.