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细菌素与饮食诱导肥胖小鼠的肠道和全身改善有关,并维持上皮屏障的完整性。

bacteriocin is associated with intestinal and systemic improvements in diet-induced obese mice and maintains epithelial barrier integrity .

机构信息

a Department of Food Science & Technology , University of California , Davis , CA, USA.

b Department of Nutrition , University of California , Davis , CA, USA.

出版信息

Gut Microbes. 2019;10(3):382-397. doi: 10.1080/19490976.2018.1534513. Epub 2018 Nov 8.

Abstract

We investigated the bacteriocin plantaricin EF (PlnEF) system for its contributions to mediated benefits in a mouse model of diet-induced obesity. C57BL/6J mice on a high-fat diet (HFD) were administered a rifampicin resistant mutant of NCMIB8826 (NICMB8826-R) or an isogenic Δ mutant strain, LM0419, every 48 h for nine weeks. Mice fed wild-type , but not LM0419, reduced their consumption of the HFD starting three weeks into the study and exhibited an overall 10% reduction in weight gain. The responses were independent of glucose homeostasis, as both NCMIB8826-R and LM0419 fed mice had improved oral glucose tolerance compared to sham controls. Although bacteriocins have antibacterial properties, the ileal, cecal, and fecal microbiota and cecocolic metabolomes were unchanged between mice fed either wild-type or the Δ mutant. Instead, only mice fed NCMIB8826-R showed an increased production of ZO-1 in ileal tissues. To verify a potential role for the plantaricin EF system in supporting intestinal epithelial function, synthesized PlnEF peptides were applied to Caco-2 cell monolayers challenged with TNF-α and IFN-γ. The combination of PlnE and PlnF were required to prevent sustained cytokine-induced losses to Caco-2 cell para- and transcellular permeability and elevated IL-8 levels. In conclusion, this study shows that probiotic ameliorates the effects of obesogenic diets through a mechanism that involves the plantaricin EF system and likely includes induced fortification of the intestinal epithelium.

摘要

我们研究了细菌素植物乳杆菌 EF(PlnEF)系统在高脂肪饮食(HFD)诱导肥胖的小鼠模型中对介导益处的贡献。将耐 rifampicin 的突变型 NCMIB8826(NICMB8826-R)或同基因 Δ突变株 LM0419 每 48 小时施用于 HFD 喂养的 C57BL/6J 小鼠,共 9 周。与喂食野生型 相比,喂食 LM0419 的小鼠从研究开始的第 3 周开始减少对 HFD 的摄入量,并表现出总体体重增加减少 10%。这些反应与葡萄糖稳态无关,因为与假对照相比,喂食 NICMB8826-R 和 LM0419 的小鼠均改善了口服葡萄糖耐量。尽管细菌素有抗菌特性,但喂食野生型或 Δ突变体的小鼠的回肠、盲肠和粪便微生物群和盲肠结肠代谢组均无变化。相反,只有喂食 NICMB8826-R 的小鼠显示回肠组织中 ZO-1 的产生增加。为了验证植物乳杆菌 EF 系统在支持肠道上皮细胞功能中的潜在作用,将合成的 PlnEF 肽应用于受到 TNF-α和 IFN-γ挑战的 Caco-2 细胞单层。PlnE 和 PlnF 的组合是预防持续的细胞因子诱导的 Caco-2 细胞旁和穿细胞通透性丧失和升高的 IL-8 水平所必需的。总之,这项研究表明,益生菌 通过涉及植物乳杆菌 EF 系统的机制改善肥胖饮食的作用,这可能包括 诱导的肠道上皮强化。

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