果胶在体外以一定程度的甲基酯化依赖方式减轻念珠菌素诱导的肠道屏障破坏和炎症

IF 5.1 Q1 CHEMISTRY, APPLIED
Naschla Gasaly , Xiaochen Chen , Luis Silva-Lagos , Isaura Beatriz Borges Silva , Marcela A. Hermoso , Paul de Vos
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引用次数: 0

摘要

果胶是一种膳食纤维,其抗炎特性受其甲基酯化程度(DM)的影响。炎症性肠病(IBD)的特征是由上皮屏障受损、微生物群失调和过度活跃的免疫反应引起的慢性炎症。除了细菌生态失调,最近的研究强调肠道菌群,特别是白色念珠菌,在IBD的进展中。白色念珠菌在IBD患者中经常升高,并分泌念珠菌素(CaLysin),这是一种破坏上皮屏障完整性的细胞溶解毒素。本研究评估了低(DM18)和高(DM88) DM的柠檬衍生果胶对calysin诱导的体外上皮应激的保护作用。在CaLysin攻毒前,用果胶对T84细胞单层进行预处理。CaLysin损伤屏障功能,增加乳酸脱氢酶(LDH)释放和促炎细胞因子(如IL-8, IL-33),同时下调紧密连接蛋白(Claudin-1, Occludin)和组织修复标志物,如视黄醛脱氢酶1 (ALDH1A1)和双调节蛋白(AREG)。两种果胶都减轻了这些影响,保持屏障完整性,减少LDH释放和细胞因子表达(例如,IL-8, IL-13, IL-18, CCL20)。果胶还以dm依赖的方式上调紧密连接蛋白(Claudin-1、Occludin、Zonula Occludens-1)的mRNA和蛋白水平,并增强组织修复基因。这些发现强调了果胶的潜力,特别是那些低dm (DM18)的果胶,在防止calysin诱导的肠道上皮损伤方面。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Pectins mitigate Candidalysin-induced gut barrier disruption and inflammation in vitro in a degree of methyl-esterification-dependent manner

Pectins mitigate Candidalysin-induced gut barrier disruption and inflammation in vitro in a degree of methyl-esterification-dependent manner
Pectin, a dietary fiber, exhibits anti-inflammatory properties influenced by its degree of methyl-esterification (DM). Inflammatory bowel disease (IBD) is characterized by chronic inflammation due to a compromised epithelial barrier, dysregulated microbiota, and an overactive immune response. Beyond bacterial dysbiosis, recent research emphasizes the gut mycobiota, particularly Candida albicans, in IBD progression. C. albicans is frequently elevated in IBD patients and secretes candidalysin (CaLysin), a cytolytic toxin that disrupts epithelial barrier integrity. This study evaluates the protective effects of lemon-derived pectins with low (DM18) and high (DM88) DM against CaLysin-induced epithelial-stress in vitro. T84 cell monolayers were pre-treated with pectins prior to CaLysin challenge. CaLysin impaired barrier function, increased lactate dehydrogenase (LDH) release, and pro-inflammatory cytokines (e.g., IL-8, IL-33), while downregulating tight junction proteins (Claudin-1, Occludin) and tissue repair markers such as Retinaldehyde dehydrogenase 1 (ALDH1A1) and Amphiregulin (AREG). Both pectins mitigated these effects, preserving barrier integrity, reducing LDH release, and cytokine expression (e.g., IL-8, IL-13, IL-18, CCL20). Pectins also upregulated tight junction proteins (Claudin-1, Occludin, Zonula Occludens-1) at mRNA and protein levels in a DM-dependent manner and enhanced tissue repair genes. These findings highlight the potential of pectins, particularly those with low-DM (DM18), in protecting against CaLysin-induced gut epithelial damage.
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来源期刊
CiteScore
4.50
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审稿时长
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