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首页> 外文期刊>Cytokine >Induction effects of Faecalibacterium prausnitzii and its extracellular vesicles on toll-like receptor signaling pathway gene expression and cytokine level in human intestinal epithelial cells
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Induction effects of Faecalibacterium prausnitzii and its extracellular vesicles on toll-like receptor signaling pathway gene expression and cytokine level in human intestinal epithelial cells

机译:粪便杆菌及其细胞外囊泡对人肠上皮细胞诱导术治疗Prausnitzii及其细胞外囊泡对人肠上皮细胞的细胞因子

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A single layer of epithelial cells creates an interface between the host and microorganisms colonizing the gastrointestinal tract. In a healthy intestine, commensal bacteria and their metabolites can interact with epithelial cells as they are identified by Toll-like receptors (TLRs); This interaction results in homeostasis and immune responses. The present study aimed at evaluating Faecalibacterium prausnitzii- and extracellular vesicles (EVs)-induced expression of involved genes in TLRs signaling pathway and cytokines production in Caco-2 cell line. In this study, Caco-2 cell line was treated with F. prausitzii and its EVs. Using the protein levels of 12 cytokines were also evaluated by ELISA assay. F. prausnitzii induced upregulation in FOS, JUN, TNF-alpha, NFKB1, TLR3, IKBKB and CD86 genes. Furthermore, stimulation of Caco-2 cells with EVs derived from F. prausnitzii induced upregulation of CXCL8, CCL2, FOS, MAP2K4, TLR7, TLR3, IRF1, NFKBIA and TNF-alpha genes. Based on ELISA assay, Caco-2 cells treated with F. prausnitzii and its EVs showed a significant increase in TNF-alpha, IL-4, IL-8, and IL-10 expression and significant decreased in IL-1, IL-2, IL-6, IL-12, IL-17a, IFN-gamma compared to the control group (P < 0.05). In conclusion, EVs derived from F. prausnitzii showed greater efficacy in decreasing the inflammatory cytokines and increasing the anti-inflammatory cytokines, compared to F. prausnitzii. Our findings can be used as a theoretical model for EVs application in the potential treatment of inflammation.
机译:一层上皮细胞在宿主和微生物之间占胃肠道的微生物之间产生界面。在健康的肠道中,共生细菌和它们的代谢物可以与上皮细胞相互作用,因为它们被损失的受体(TLR)鉴定;这种相互作用导致稳态和免疫反应。目前的研究旨在评估Prausnitzii和细胞外囊泡和细胞外囊泡(EVS)的诱导基因在TLR信号通路和细胞因子在Caco-2细胞系中产生的表达。在该研究中,CaCO-2细胞系用F.Prausitzii及其动力处理。使用ELISA测定还评估使用12个细胞因子的蛋白质水平。 F. Prausnitzii诱导FOS,Jun,TNF-alpha,NFKB1,TLR3,IKBKB和CD86基因的上调。此外,通过衍生自F.Prausnitzii的EVS诱导CXCL8,CCL2,FOS,MAP2K4,TLR7,TLR3,IRF1,NFKBIA和TNF-α基因的EVS刺激CaCo-2细胞。基于ELISA测定,用F.Prausnitzii及其EV处理的Caco-2细胞显示TNF-α,IL-4,IL-8和IL-10表达显着增加,IL-1,IL-2的显着降低与对照组相比,IL-6,IL-12,IL-17A,IFN-GAMMA(P <0.05)。总之,与F.Prausnitzii相比,Prausnitzii衍生自F.Prausnitzii的EVS表现出更高的疗效,并增加抗炎细胞因子。我们的发现可以用作EVS应用在炎症潜在治疗中的理论模型。

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