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从伊豆-赤泽深海海水中分离得到的新菌株 BF1-13 产生的代谢产物可保护肠道上皮屏障免受过氧化氢诱导的功能障碍。

Metabolites Produced by a New Strain BF1-13 Isolated from Deep Seawater of Izu-Akazawa Protect the Intestinal Epithelial Barrier from the Dysfunction Induced by Hydrogen Peroxide.

机构信息

Applied Microbiology Lab, Course of Applied Marine Biosciences, Graduate School of Marine Science and Technology, Tokyo University of Marine Science and Technology, Tokyo 108-8477, Japan.

DSW Laboratory of DHC Co., Ltd., Tokyo 106-0047, Japan.

出版信息

Mar Drugs. 2022 Jan 20;20(2):87. doi: 10.3390/md20020087.

DOI:10.3390/md20020087
PMID:35200617
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8878880/
Abstract

This study aimed to investigate the protective effect of the metabolites produced by a new strain BF1-13, isolated from deep seawater (DSW), on the intestinal epithelial barrier against the dysfunction induced by hydrogen peroxide (HO) 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 HO 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 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 HO intracellular invasion into Caco-2 cells. This is the first report on the enhancement of TJs by LA produced by LAB.

摘要

本研究旨在探讨一种从深海(DSW)中分离的新菌株 BF1-13 产生的代谢产物对肠道上皮屏障的保护作用,以防止其免受过氧化氢(HO)引起的功能障碍,并阐明其作用机制。通过跨上皮电阻(TEER)研究了 BF1-13 代谢产物对 HO 处理的肠道上皮模型屏障功能的保护作用。代谢产物通过免疫荧光染色和定量 RT-PCR 增强了紧密连接蛋白 4(CLDN-4)的表达,包括转录水平。代谢产物还显示出对水通道蛋白 3(AQP3)表达的抑制。该同型发酵乳酸菌(LAB)产生的乳酸(LA)对 CLDN-4 表达也有类似的增强作用。BF1-13 菌株的代谢产物通过 LA 增强紧密连接(TJ),同时抑制 AQP3 促进 HO 细胞内入侵 Caco-2 细胞,从而减轻肠道上皮屏障功能障碍。这是 LAB 产生的 LA 增强 TJ 的首次报道。

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