Abstract
This study aimed to investigate the protective effect of the metabolites produced by a new Lactiplantibacillus plantarum strain BF1-13, isolated from deep seawater (DSW), on the intestinal epithelial barrier against the dysfunction induced by hydrogen peroxide (H2O2) and to elucidate the mechanism underlying the effect. Protective effect of the metabolites by strain BF1-13 on the barrier function of the intestinal epithelial model treated with H2O2 was investigated by the transepithelial electrical resistance (TEER). The metabolites enhanced the Claudin-4 (CLDN-4) expression, including at the transcription level, indicated by immunofluorescence staining and quantitative RT-PCR. The metabolites also showed a suppression of aquaporin3 (AQP3) expression. Lactic acid (LA) produced by this strain of homofermentative lactic acid bacteria (LAB) had a similar enhancement on CLDN-4 expression. The metabolites of L. plantarum strain BF1-13 alleviated the dysfunction of intestinal epithelial barrier owing to its enhancement on the tight junctions (TJs) by LA, along with its suppression on AQP3-facilitating H2O2 intracellular invasion into Caco-2 cells. This is the first report on the enhancement of TJs by LA produced by LAB.
Highlights
This study aims to investigate the protective effect of the metabolites produced by deep seawater (DSW)-derived L. plantarum strain BF1-13 on the intestinal epithelial barrier against the
Metabolites produced by DSW-derived Lactiplantibacillus plantarum strain
The oxidative stress induced by H2 O2 impairs the intestinal epithelial barrier function which is mainly regulated by tight junctions (TJs), especially CLDN-4 [26]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. It is known that the intestinal epithelium basically functions for the maintenance of the internal environment [1]. It absorbs nutrients and defends the exogenous pathogens and their secretion of toxins to protect the human body from diseases, including inflammatory bowel disease (IBD), celiac diseases, and diarrhea [2]. Between the intestinal epithelial cells, there exist TJs mediating the paracellular permeability to achieve the barrier function
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