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首页> 外文期刊>Infection and immunity >Antisecretory Factor Peptide AF-16 Inhibits the Secreted Autotransporter Toxin-Stimulated Transcellular and Paracellular Passages of Fluid in Cultured Human Enterocyte-Like Cells
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Antisecretory Factor Peptide AF-16 Inhibits the Secreted Autotransporter Toxin-Stimulated Transcellular and Paracellular Passages of Fluid in Cultured Human Enterocyte-Like Cells

机译：抗分泌因子肽AF-16抑制培养的人肠上皮样细胞中分泌的自转运毒素刺激的细胞跨细胞和旁细胞通道。

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摘要

Both the endogenous antisecretory factor (AF) protein and peptide AF-16, which has a sequence that matches that of the active N-terminal region of AF, inhibit the increase in the epithelial transport of fluid and electrolytes induced by bacterial toxins in animal and ex vivo models. We conducted a study to investigate the inhibitory effect of peptide AF-16 against the increase of transcellular passage and paracellular permeability promoted by the secreted autotransporter toxin (Sat) in a cultured cellular model of the human intestinal epithelial barrier. Peptide AF-16 produced a concentration-dependent inhibition of the Sat-induced increase in the formation of fluid domes, in the mucosal-to-serosal passage of d-[1-14C]mannitol, and in the rearrangements in the distribution and protein expression of the tight junction (TJ)-associated proteins ZO-1 and occludin in cultured human enterocyte-like Caco-2/TC7 cell monolayers. In addition, we show that peptide AF-16 also inhibits the cholera toxin-induced increase of transcellular passage and the Clostridium difficile toxin-induced effects on paracellular permeability and TJ protein organization in Caco-2/TC7 cell monolayers. Treatment of cell monolayers by the lipid raft disorganizer methyl-β-cyclodextrin abolished the inhibitory activity of peptide AF-16 at the transcellular passage level and did not modify the effect of the peptide at the paracellular level.
机译：内源性抗分泌因子（AF）蛋白和肽AF-16具有与AF的活性N端区域相匹配的序列，可抑制动物和动物体内细菌毒素诱导的液体和电解质的上皮运输增加。离体模型。我们进行了一项研究，以研究在人类肠道上皮屏障的培养细胞模型中，AF-16肽对分泌的自转运毒素（Sat）促进的跨细胞传代和副细胞通透性增加的抑制作用。 AF-16肽对Sat诱导的液体穹顶形成，d- [1-14C]甘露醇的黏膜至浆膜通道以及分布和蛋白质的重排产生浓度依赖性抑制作用紧密连接（TJ）相关蛋白ZO-1和闭合蛋白在培养的人肠上皮样Caco-2 / TC7细胞单层中的表达。此外，我们表明，肽AF-16还抑制霍乱毒素诱导的跨细胞传代的增加以及艰难梭菌毒素诱导的对Caco-2 / TC7细胞单层细胞旁通透性和TJ蛋白组织的影响。用脂质筏分解剂甲基-β-环糊精处理细胞单层消除了肽AF-16在跨细胞传代水平上的抑制活性，并且没有改变肽在细胞旁水平上的作用。

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