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Updated: Jan 1, 2026

In Vitro and In Vivo Approaches to Determine Intestinal Epithelial Cell Permeability
Published on: October 19, 2018
Farnesol contributes to intestinal epithelial barrier function by enhancing tight junctions via the JAK/STAT3
Yangxin Fang1, Chunrong Wu1, Qiuyue Wang1
1Department of Trauma-Emergency & Critical Care Medicine Shanghai Fifth People's Hospital, Fudan University, Minhang district, 200240, Shanghai, China.
Abstract:
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.
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