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首页> 外文期刊>European cytokine network >Neutrophil F-actin and myosin but not microtubules functionally regulate transepithelial migration induced by interleukin 8 across a cultured intestinal epithelial monolayer.
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Neutrophil F-actin and myosin but not microtubules functionally regulate transepithelial migration induced by interleukin 8 across a cultured intestinal epithelial monolayer.

机译：中性粒细胞F-肌动蛋白和肌球蛋白，而非微管在功能上调节由白介素8诱导的跨上皮肠上皮单层的跨上皮迁移。

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摘要

The role of the polymorphonuclear leukocyte (PMN) cytoskeleton during the transmigration across colonic epithelial cells is not very well understood. In order to study the role of different components of the PMN cytoskeleton during transepithelial migration across a colonic epithelial cell monolayer (T84), PMN were preincubated with drugs affecting either the actin cytoskeleton (cytochalasin B, iota toxin of Clostridium perfringens, and phalloidin) or the microtubules (colchicine and taxol). The role of PMN myosin during transepithelial migration was investigated using the inhibitor 2,3-butanedione monoxime (BDM) and DC3B toxin. PMN intracellular Ca2+, during neutrophil adhesion and translocation across the epithelium, was assessed by the Ca2+ chelator 1, 2bis-(2-aminophenoxy)-ethane-N,N,N', N'-tetra-acetic acid tetrakis (acetoxymethyl) ester (BAPTA-AM). Transmigration of PMN was initiated by applying either interleukin-8 or formyl-met-leu-phe (fMLP). While colchicine and taxol preexposure did not influence PMN transepithelial migration, treatment with cytochalasin B, iota toxin, phalloidin, BDM, DC3B toxin and BAPTA-AM greatly diminished migration of PMN across T84 monolayers. Similarly, cell-cell contacts established between PMN and epithelial cells during the transmigration were diminished after treatment of PMN with iota toxin or cytochalasin B. These data show that the neutrophil actin cytokeleton and myosin, but not the microtubules, evoke a Ca2+ -dependent motility that facilitates migration across the colonic epithelial barrier.
机译：跨结肠上皮细胞的迁移过程中，多形核白细胞（PMN）细胞骨架的作用还不是很清楚。为了研究PMN细胞骨架的不同成分在跨结肠上皮细胞单层（T84）跨上皮迁移过程中的作用，将PMN与影响肌动蛋白细胞骨架（细胞松弛素B，产气荚膜梭状芽孢杆菌的Iota毒素和鬼笔环肽）的药物预孵育或微管（秋水仙碱和紫杉醇）。 PMN肌球蛋白在上皮迁移过程中的作用是使用抑制剂2,3-丁二酮单肟（BDM）和DC3B毒素进行的。在中性粒细胞粘附和跨上皮转运过程中，PMN胞内Ca2 +由Ca2 +螯合剂1，2双-（2-氨基苯氧基）-乙烷-N，N，N'，N'-四乙酸四（乙酰氧基甲基）酯评估（BAPTA-AM）。通过应用白介素8或甲酰-met-leu-phe（fMLP）启动PMN的迁移。虽然秋水仙碱和紫杉醇暴露前不影响PMN跨上皮迁移，但用细胞松弛素B，iota毒素，鬼笔环肽，BDM，DC3B毒素和BAPTA-AM处理可大大减少PMN跨T84单层的迁移。类似地，在用异位毒素或细胞松弛素B治疗PMN后，在迁移过程中PMN与上皮细胞之间建立的细胞间接触减少。这些数据表明嗜中性白细胞肌动蛋白细胞骨架和肌球蛋白（而非微管）引起Ca2 +依赖性运动促进跨结肠上皮屏障的迁移。

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