Candida albicans causes mucosal diseases and secretes farnesol, a quorum-sensing molecule, which plays a vital role in suppressing the yeast-to-mycelia switch. Farnesol can also regulate immune cell function. However, how farnesol interacts with the intestinal epithelium remains unknown. Herein, we identified that farnesol promotes intestinal barrier function, by promoting transepithelial electrical resistance, reducing paracellular flux, inducing the Zonula Occludens-1 Protein (ZO-1) and occludin expression. Moreover, the JAK/STAT3 signaling pathway was activated after farnesol treatment, and inhibition of STAT3 phosphorylation by stattic remarkably suppressed the expression level of ZO-1. Additionally, chromatin immunoprecipitation assay (Chip) revealed that farnesol facilitated the transcriptional activation of STAT3 to significantly enhance the expression of ZO-1. Taken together, our findings demonstrated that farnesol facilitated intestinal epithelial barrier transcriptional regulation via activating JAK/STAT3 signaling. The involved molecules may be potentially targeted for treatment of Candida albicans invasion.

中文翻译：

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法尼醇通过在分化的Caco-2细胞中通过JAK / STAT3信号通路增强紧密连接，从而有助于肠道上皮屏障功能。

白色念珠菌可引起粘膜疾病并分泌法尼醇（一种群体感应分子），在抑制酵母菌丝状体转换方面起着至关重要的作用。法尼醇还可以调节免疫细胞功能。然而，法尼醇如何与肠上皮相互作用仍然是未知的。在本文中，我们确定了法尼醇通过促进跨上皮电阻，减少细胞旁通量，诱导Zonula Occludens-1蛋白（ZO-1）和occludin表达来促进肠屏障功能。此外，法呢醇处理后，JAK / STAT3信号通路被激活，并且由STAT抑制STAT3磷酸化显着抑制了ZO-1的表达水平。此外，染色质免疫沉淀试验（Chip）显示，法尼醇可促进STAT3的转录激活，从而显着增强ZO-1的表达。两者合计，我们的研究结果表明，法尼醇通过激活JAK / STAT3信号传导促进肠道上皮屏障转录调控。涉及的分子可能被潜在地靶向治疗白色念珠菌入侵。