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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Resveratrol modulates the gut microbiota to prevent murine colitis development through induction of Tregs and suppression of Th17 cells
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Resveratrol modulates the gut microbiota to prevent murine colitis development through induction of Tregs and suppression of Th17 cells

机译：白藜芦醇调节肠道微生物，通过诱导Tregs和Th17细胞的抑制来防止鼠结肠炎开发

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Abstract Inflammatory diseases of the gastrointestinal tract are often associated with microbial dysbiosis. Thus, dietary interactions with intestinal microbiota, to maintain homeostasis, play a crucial role in regulation of clinical disorders such as colitis. In the current study, we investigated if resveratrol, a polyphenol found in a variety of foods and beverages, would reverse microbial dysbiosis induced during colitis. Administration of resveratrol attenuated colonic inflammation and clinical symptoms in the murine model of 2,4,6‐trinitrobenzenesulfonic acid (TNBS)‐induced colitis. Resveratrol treatment in mice with colitis led to an increase in CD4 + FOXP3 + and CD4 + IL‐10 + T cells, and a decrease in CD4 + IFN‐γ + and CD4 + IL‐17 + T cells. 16S rRNA gene sequencing to investigate alterations in the gut microbiota revealed that TNBS caused significant dysbiosis, which was reversed following resveratrol treatment. Analysis of cecal flush revealed that TNBS administration led to an increase in species such as Bacteroides acidifaciens , but decrease in species such as Ruminococcus gnavus and Akkermansia mucinphilia , as well as a decrease in SCFA i ‐butyric acid. However, resveratrol treatment restored the gut bacteria back to homeostatic levels, and increased production of i‐butyric acid. Fecal transfer experiments confirmed the protective role of resveratrol‐induced microbiota against colitis inasmuch as such recipient mice were more resistant to TNBS‐colitis and exhibited polarization toward CD4 + FOXP3 + T cells and decreases in CD4 + IFN‐γ + and CD4 + IL‐17 + T cells. Collectively, these data demonstrate that resveratrol‐mediated attenuation of colitis results from reversal of microbial dysbiosis induced during colitis and such microbiota protect the host from colonic inflammation by inducing Tregs while suppressing inflammatory Th1/Th17 cells.
机译：胃肠道的抽象炎症疾病通常与微生物消化不良有关。因此，与肠道微生物生物的膳食相互作用，以维持稳态，在调节结肠炎等临床疾病中起至关重要的作用。在目前的研究中，我们研究了在各种食品和饮料中发现的多酚，将逆转结肠炎诱导的微生物脱泻病。将白藜芦醇施用在2,4,6-三硝基磺酸（TNBS）诱导的结肠炎的小鼠模型中减毒结肠炎症和临床症状。白癜风在具有结肠炎的小鼠中治疗导致CD4 + Foxp3 +和CD4 + IL-10 + T细胞的增加，以及CD4 + IFN-γ+和CD4 + IL-17 + T细胞的降低。 16S RRNA基因测序以研究肠道微生物群的改变，显示TNB引起了显着的消化不良，在白藜芦醇治疗后逆转。 Cechal Flush分析显示，TNBS给药导致诸如菌酸等种类的种类的增加，但是喇菇和Akkermansia粘片等物种的降低，以及SCFA I-丁酸的降低。然而，白藜芦醇治疗将肠道细菌恢复到稳态水平，并增加了I-丁酸的产量。粪便转移实验证实了白藜芦醇诱导的微生物生物的保护作用，因为这种受体小鼠更抗TNBS-结肠炎，并向CD4 + FoxP3 + T细胞显示出偏振，并降低CD4 + IFN-γ+和CD4 + IL- 17 + T细胞。总的来说，这些数据表明，白藜芦醇介导的结肠炎的衰减因结肠炎和这种微生物瘤期间诱导的微生物缺陷症的逆转导致通过诱导Tregs在抑制炎症Th117细胞的同时保护宿主免受结肠炎症。

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