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首页> 外文期刊>Physiological Reports >Effects of Lactobacillus johnsonii and Lactobacillus reuteri on gut barrier function and heat shock proteins in intestinal porcine epithelial cells
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Effects of Lactobacillus johnsonii and Lactobacillus reuteri on gut barrier function and heat shock proteins in intestinal porcine epithelial cells

机译：约翰逊氏乳杆菌和罗伊氏乳杆菌对肠道猪上皮细胞肠道屏障功能和热休克蛋白的影响

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AbstractHeat shock proteins (HSPs) are a set of highly conserved proteins that can serve as intestinal gate keepers in gut homeostasis. Here, effects of a probiotic, Lactobacillus rhamnosus GG (LGG), and two novel porcine isolates, Lactobacillus johnsonii strain P47-HY and Lactobacillus reuteri strain P43-HUV, on cytoprotective HSP expression and gut barrier function, were investigated in a porcine IPEC-J2 intestinal epithelial cell line model. The IPEC-J2 cells polarized on a permeable filter exhibited villus-like cell phenotype with development of apical microvilli. Western blot analysis detected HSP expression in IPEC-J2 and revealed that L. johnsonii and L. reuteri strains were able to significantly induce HSP27, despite high basal expression in IPEC-J2, whereas LGG did not. For HSP72, only the supernatant of L. reuteri induced the expression, which was comparable to the heat shock treatment, which indicated that HSP72 expression was more stimulus specific. The protective effect of lactobacilli was further studied in IPEC-J2 under an enterotoxigenic Escherichia coli (ETEC) challenge. ETEC caused intestinal barrier destruction, as reflected by loss of cell–cell contact, reduced IPEC-J2 cell viability and transepithelial electrical resistance, and disruption of tight junction protein zonula occludens-1. In contrast, the L. reuteri treatment substantially counteracted these detrimental effects and preserved the barrier function. L. johnsonii and LGG also achieved barrier protection, partly by directly inhibiting ETEC attachment. Together, the results indicate that specific strains of Lactobacillus can enhance gut barrier function through cytoprotective HSP induction and fortify the cell protection against ETEC challenge through tight junction protein modulation and direct interaction with pathogens.
机译：摘要热休克蛋白（HSP）是一组高度保守的蛋白，可以作为肠道稳态的肠道门将。在这里，在猪的IPEC中研究了益生菌鼠李糖乳杆菌GG（LGG）和两种新型猪隔离株，即约翰逊乳杆菌P47-HY和路氏乳杆菌P43-HUV对细胞保护性HSP表达和肠屏障功能的影响。 J2肠上皮细胞系模型。在可渗透滤膜上极化的IPEC-J2细胞表现出绒毛样细胞表型，并伴有顶端微绒毛。蛋白质印迹分析检测到IPEC-J2中的HSP表达，并显示尽管在IPEC-J2中基础表达很高，但约翰逊氏菌和罗伊氏乳杆菌菌株仍能显着诱导HSP27，而LGG则没有。对于HSP72，只有罗伊氏乳杆菌的上清液诱导表达，这与热休克处理相当，这表明HSP72的表达更具刺激特异性。在IPEC-J2中，在产肠毒素的大肠杆菌（ETEC）攻击下进一步研究了乳杆菌的保护作用。 ETEC引起肠壁屏障破坏，表现为细胞与细胞接触的丧失，IPEC-J2细胞活力的降低和跨上皮电阻的降低以及紧密连接蛋白小带闭塞1的破坏。相反，路氏乳杆菌的治疗基本上抵消了这些有害作用并保留了屏障功能。约翰逊氏菌和LGG还通过直接抑制ETEC附着来实现屏障保护。总之，结果表明，乳酸杆菌的特定菌株可以通过细胞保护性HSP诱导增强肠屏障功能，并通过紧密连接蛋白调节和与病原体的直接相互作用来增强针对ETEC攻击的细胞保护作用。

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