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Mechanisms of neutrophil transmigration across renal proximal tubular HK-2 cells

机译：嗜中性粒细胞跨肾近端肾小管HK-2细胞迁移的机制

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Background: Adhesion of intratubular leukocytes to proximal tubules in biopsies of patients with rapidly progressive glomerulonephritis and the appearance of leukocytes in the urine in interstitial nephritis suggest interactions between leukocytes and tubular epithelia in renal diseases. The aim of this study was to investigate the effect of cytokines and endotoxin on leukocyte migration through proximal tubular epithelial cells and also to determine the role of the transmembrane adhesion molecules ICAM-1 and CD47 in this process. Methods: Experiments determined transepithelial migration (TEM) of PMN (polymorphonuclear) leukocytes through monolayers, of HK-2. Expression of ICAM-1 and CD47 was assessed via confocal immunofluorescence, FACS analysis and western blotting. The effect of antibodies against ICAM-1 and CD47 on TEM was examined. Furthermore measurements of cytokine release (IL6 and IL-8) were performed. Results: Preincubation of HK-2 cells with either TNF alpha or LIPS resulted in stimulation of PMN migration through monolayers of HK-2 cells. There was no preferred direction of transmigration. ICAM-1 was expressed by HK-2 cells and expression was increased after 4 h stimulation with TNFa or LPS. Application of ICAM-1 antibodies inhibited TEM. CD47 was expressed in both HK-2 cells and PMN. CD47 antibodies inhibited predominantly basolateral-to-apical TEM. HK-2 cells released IL-8 and IL-6 preferably into the apical compartment. Additionally, we showed that fMLP induced transmigration through monolayers of HK-2 cells was associated with significant increased CD47 expression on PMN cell surfaces. Conclusions: Inflammatory mediators stimulate TEM of PMN through monolayers of HK-2 cells without a clearly discernible preference of direction. Mechanisms involved in TEM stimulated by cytokines or endotoxin appear to be mainly changes in surface receptor densities of HK-2 cells with ICAM-1 and CD47 playing an essential role. Copyright (c) 2006 S. Karger AG, Basel.
机译：背景：在快速进展性肾小球肾炎患者的活检中，小管内白细胞与近端小管的粘附以及间质性肾炎尿液中白细胞的出现表明肾脏疾病中白细胞与肾小管上皮之间的相互作用。这项研究的目的是研究细胞因子和内毒素对白细胞通过近端肾小管上皮细胞迁移的影响，并确定跨膜粘附分子ICAM-1和CD47在此过程中的作用。方法：实验确定了PMN（多形核）白细胞通过单层HK-2的跨上皮迁移（TEM）。通过共聚焦免疫荧光，FACS分析和蛋白质印迹评估ICAM-1和CD47的表达。检查了针对ICAM-1和CD47的抗体对TEM的影响。此外，进行了细胞因子释放（IL6和IL-8）的测量。结果：HK-2细胞与TNFα或LIPS的预孵育导致刺激PMN通过HK-2细胞单层迁移。没有首选的迁移方向。 ICAM-1由HK-2细胞表达，并在用TNFa或LPS刺激4 h后表达增加。 ICAM-1抗体的应用抑制了TEM。 CD47在HK-2细胞和PMN中均表达。 CD47抗体主要抑制基底外侧至顶端TEM。 HK-2细胞优选将IL-8和IL-6释放至顶端区室。此外，我们显示fM​​LP诱导通过HK-2细胞单层的迁移与PMN细胞表面CD47表达的显着增加有关。结论：炎性介质通过HK-2细胞单层刺激PMN的TEM，而没有明显的方向偏好。细胞因子或内毒素刺激的TEM中涉及的机制似乎主要是HK-2细胞表面受体密度的变化，ICAM-1和CD47起着重要作用。版权所有（c）2006 S. Karger AG，巴塞尔。

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