INTERLEUKIN-8 IS A POTENT MEDIATOR OF EOSINOPHIL CHEMOTAXIS THROUGH ENDOTHELIUM AND EPITHELIUM

INTERLEUKIN-8 IS A POTENT MEDIATOR OF EOSINOPHIL CHEMOTAXIS THROUGH ENDOTHELIUM AND EPITHELIUM
复制标题

DOI:
10.1152/ajplung.1995.268.1.l117
复制
发表时间:
1995-01-01
影响因子:
4.9
通讯作者:
CASALE, TB
CASALE, TB
中科院分区:
医学2区
文献类型:
--
作者:
ERGER, RA;CASALE, TB

文献摘要

被引文献

相似文献

白细胞介素-8 (IL-8)是一种有效的促炎细胞因子,已被证明对中性粒细胞、淋巴细胞和嗜碱性粒细胞具有趋化活性。IL-8对嗜酸性粒细胞趋化性的影响尚不清楚。由于嗜酸性粒细胞在过敏性炎症部位积聚,并可能在哮喘发病机制中发挥作用,我们研究了IL-8的嗜酸性粒细胞能力。我们检测了IL-8诱导人嗜酸性粒细胞通过3 μ m孔裸滤膜迁移的能力,以及在这些滤膜上培养的人脐静脉内皮细胞和人肺ii型样上皮细胞(A549)单层细胞迁移的能力。IL-8诱导了类似剂量相关的嗜酸性粒细胞通过所有三个屏障的迁移。动力学实验表明,通过非细胞屏障的迁移速度更快,但在3小时内通过所有屏障的迁移速度相当。趋化/趋化动力学数据表明,il -8诱导的嗜酸性粒细胞迁移是趋化的。我们还确定,与其他细胞因子相比,IL-8诱导跨细胞迁移的能力是独一无二的,并且不依赖于使用新鲜或传代单层细胞作为屏障。因此,我们的数据表明,IL-8可能在过敏性呼吸道疾病中观察到的组织嗜酸性粒细胞增多中起重要作用。
Interleukin-8 (IL-8), a potent pro-inflammatory cytokine, has been shown to have chemotactic activity for neutrophils, lymphocytes, and basophils. Effects of IL-8 on eosinophil chemotaxis are unresolved. Because eosinophils accumulate at the site of allergic inflammation and may play a role in the pathogenesis of asthma, we investigated the eosinophilotactic capacity of IL-8. We examined the ability of IL-8 to induce human eosinophil migration across 3-mu m pore naked filters, and human umbilical vein endothelial cell and human pulmonary type II-like epithelial cell (A549) monolayers cultured on these filters. IL-8 induced similar dose-related eosinophil migration through all three barriers. Kinetic experiments indicated more rapid migration through noncellular barriers but equivalent migration through all barriers by 3 h. Chemotactic/chemokinetic data show that IL-8-induced eosinophil migration is chemotactic. We also determined that the ability of IL-8 to induce transcellular migration was unique in comparison with other cytokines and was not dependent on the use of fresh vs. passaged monolayer cells as barriers. Therefore our data indicate that IL-8 may play a significant role in tissue eosinophilia observed in allergic respiratory diseases.