Neutrophil transmigration across human airway epithelial monolayers - Mechanisms and dependence on electrical resistance
Neutrophil transmigration across human airway epithelial monolayers - Mechanisms and dependence on electrical resistance
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DOI：
10.1165/ajrcmb.23.3.4068
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发表时间：
2000-09-01
影响因子：
6.4
通讯作者：
Proud, D
中科院分区：
文献类型：
--
作者：
Kidney, JC;Proud, D
为了检测中性粒细胞从基底侧到腔内方向的跨上皮迁移，在可透性支架下表面的空气-介质界面上培养支气管上皮细胞（16HBE），在测量2小时内中性粒细胞迁移之前，记录每层膜上的阻力。亚融合单层（阻力< 250 ω）允许中性粒细胞高度自发迁移（7.4 +/- 1%）。白细胞介素(IL)-8 （100 ng/ml）进一步增强（29.7 +/- 3%）。融合单层（250 - 700 ω）显示低自发迁移（2 +/- 0.5%），但对IL-8有明显反应（12.4 +/- 1.3%）。在培养中，16HBE抗性继续增加，并与最小的自发迁移（0.5%）或对IL-8的反应相关。使用250 - 700 hi范围内的细胞，中性粒细胞向IL-8的迁移是剂量依赖性的，当上皮细胞与肿瘤坏死因子- α和干扰素- γ联合孵卵时，中性粒细胞向IL-8的迁移是刺激特异性的，并且通过上皮细胞与F(ab)(2)抗细胞间粘附分子(ICAM)-1或中性粒细胞与抗cd18、抗cd11a、抗cd11b或抗cd11c预孵卵而减少，但不通过抗cd11d。表明β(2)-整合素- icam -1相互作用在迁移过程中起作用。
To examine neutrophil transepithelial migration in the basolateral-to-luminal direction, bronchial epithelial cells (16HBE) were grown at an air-medium interface on the lower face of permeable supports, and resistance across each membrane was recorded before measuring neutrophil transmigration over 2 h. Subconfluent monolayers (resistance < 250 Omega) permitted high spontaneous migration of neutrophils (7.4 +/- 1%), which was further enhanced (29.7 +/- 3%) in response to interleukin (IL)-8 (100 ng/ml). Confluent monolayers (250 to 700 Omega) showed low spontaneous migration (2 +/- 0.5%) but responded markedly to IL-8 (12.4 +/- 1.3%). Left in culture, 16HBE resistances continued to increase and were associated with minimal spontaneous migration (( 0.5%) or responses to IL-8. Using cells in the 250 to 700 hi range, neutrophil migration to IL-8 was dose-dependent and was enhanced when epithelial cells were incubated with a combination of tumor necrosis factor-alpha and interferon-gamma, Neutrophil migration was stimulus-specific and was reduced by preincubation of epithelial cells with a F(ab')(2) anti-intercellular adhesion molecule (ICAM)-1, or by preincubation of neutrophils with anti-CD18, anti-CD11a, anti-CD11b, or anti-CD11c, but not by anti-CD11d, indicating a role for beta(2)-integrin-ICAM-1 interaction in the migration process.