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首页> 外文期刊>Life sciences >Effects of endocytosis inhibitors on internalization of human IgG by Caco-2 human intestinal epithelial cells.
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Effects of endocytosis inhibitors on internalization of human IgG by Caco-2 human intestinal epithelial cells.

机译：内吞抑制剂对Caco-2人肠上皮细胞对人IgG内在化的影响。

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AIMS: The purpose of this study was to characterize the internalization mechanism of human IgG into the epithelial cells of human small intestine, employing human intestinal epithelial cell line Caco-2 as an in vitro model system. MAIN METHODS: Real-time PCR analysis and uptake studies of fluorescein isothiocyanate-labeled IgG (FITC-IgG) from human serum were performed using Caco-2 cells. KEY FINDINGS: Real-time PCR analysis showed that mRNA level of the neonatal Fc receptor (FcRn) was increased during the differentiation process in Caco-2 cells. The binding of FITC-labeled human IgG to the membrane surface of Caco-2 cells increased with a decrease in pH of incubation buffer. The uptake of FITC-IgG was also stimulated at acidic pH and was time-dependent. The binding and uptake of FITC-IgG at pH 6.0 was partially, but significantly, decreased by human gamma-globulin in a concentration-dependent manner. A mixture of metabolic inhibitors (sodium azide and 2-deoxyglucose) significantly inhibited the uptake, but not the binding, of FITC-IgG. In addition, endosomal acidification inhibitors such as bafilomycin A(1) and chloroquine significantly increased the accumulation of FITC-IgG. Clathrin-dependent endocytosis inhibitors (phenylarsine oxide and chlorpromazine) and caveolin-dependent endocytosis inhibitors (nystatin and indomethacin) did not decrease the uptake of FITC-IgG at pH 6.0. In contrast, macropinocytosis inhibitors such as cytochalasin B and 5-(N-ethyl-N-isopropyl) amiloride significantly decreased the uptake of FITC-IgG at pH 6.0. SIGNIFICANCE: The internalization of human IgG in human intestine might be, at least in part, due to FcRn-mediated endocytosis, which could occur by a process other than clathrin- and caveolin-dependent mechanisms.
机译：目的：本研究的目的是利用人肠上皮细胞系Caco-2作为体外模型系统，表征人IgG进入人小肠上皮细胞的内在化机制。主要方法：使用Caco-2细胞对人血清中的荧光素异硫氰酸酯标记的IgG（FITC-IgG）进行实时PCR分析和摄取研究。主要发现：实时PCR分析表明，在Caco-2细胞分化过程中，新生儿Fc受体（FcRn）的mRNA水平升高。 FITC标记的人IgG与Caco-2细胞膜表面的结合随着孵育缓冲液pH值的降低而增加。在酸性pH下，FITC-IgG的摄取也受到刺激，并且是时间依赖性的。在pH 6.0时，FITC-IgG的结合和摄取被人γ-球蛋白以浓度依赖的方式部分但显着降低。代谢抑制剂（叠氮化钠和2-脱氧葡萄糖）的混合物可显着抑制FITC-IgG的摄取，但不能抑制其结合。此外，内体酸化抑制剂，如bafilomycin A（1）和氯喹显着增加了FITC-IgG的积累。网格蛋白依赖性内吞抑制剂（苯ar氧化物和氯丙嗪）和小孔蛋白依赖性内吞抑制剂（制霉菌素和消炎痛）在pH 6.0时不会降低FITC-IgG的吸收。相反，巨胞饮抑制剂例如细胞松弛素B和5-（N-乙基-N-异丙基）阿米洛利在pH 6.0时显着降低了FITC-IgG的摄取。意义：人肠道中人IgG的内在化至少部分是由于FcRn介导的内吞作用，这可能是由于网格蛋白和小窝蛋白依赖性机制以外的其他过程所致。

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