Distinctive probiotic features share common TLR2‐dependent signalling in intestinal epithelial cells

The underlying mechanisms of probiotics and postbiotics are not well understood, but it is known that both affect the adaptive and innate immune responses. In addition, there is a growing concept that some probiotic strains have common core mechanisms that provide certain health benefits. Here, we aimed to elucidate the signalization of the probiotic bacterial strains Lactobacillus paragasseri K7, Limosilactobacillus fermentum L930BB, Bifidobacterium animalis subsp. animalis IM386 and Lactiplantibacillus plantarum WCFS1. We showed in in vitro experiments that the tested probiotics exhibit common TLR2‐ and TLR10‐dependent downstream signalling cascades involving inhibition of NF‐κB signal transduction. Under inflammatory conditions, the probiotics activated phosphatidylinositol 3‐kinase (PI3K)/Akt anti‐apoptotic pathways and protein kinase C (PKC)‐dependent pathways, which led to regulation of the actin cytoskeleton and tight junctions. These pathways contribute to the regeneration of the intestinal epithelium and modulation of the mucosal immune system, which, together with the inhibition of canonical TLR signalling, promote general immune tolerance. With this study we identified shared probiotic mechanisms and were the first to pinpoint the role of anti‐inflammatory probiotic signalling through TLR10.     

益生菌、益生元和后生元对食物过敏的影响和作用机制

食物过敏(food allergy,FA)的发病率在近二十年来持续上升,已经严重影响患者的生活质量.生命早期接触外源性抗原少而导致的免疫耐受限制是FA的主要原因.微生物-宿主的相互作用与FA密切相关,健康的微生物菌群促进宿主在生命早期建立成熟的免疫系统,减少FA的易感性,因此,改善肠道菌群和调节机体免疫在治疗FA中至关...     

Cell-free culture supernatant of Lactobacillus curvatus Wikim38 inhibits RANKL-induced osteoclast differentiation and ameliorates bone loss in ovariectomized mice

This study was conducted to investigate the inhibitory effects of the cell-free culture supernatant of Lactobacillus curvatus Wikim 38 (LC38-CS) on RANKL-induced osteoclast differentiation and bone loss in a mice model of ovariectomy-induced post-menopausal osteoporosis. LC38-CS inhibited the RANKL-induced differentiation of bone marrow-derived macrophages (BMDMs) into osteoclasts in a dose-dependent manner. F-actin ring formation and bone resorption were also reduced by LC38-CS treatment of RANKL-treated BMDMs. In addition, LC38-CS decreased the RANKL-induced activation of the TRAF6/NF-κB/MAPKs axis at the early stage and the expression of osteoclastogenesis-related genes in BMDMs treated with RANKL. PRMT1 and ADMA levels, new biomarkers for osteoclastogenesis, were decreased by LC38-CS treatment. The administration of LC38-CS increased bone volume and bone mineral density in ovariectomized mice in μ-CT analysis. These findings suggest that LC38-CS inhibited RANKL-induced osteoclast differentiation by the downregulation of molecular mechanisms and exerted anti-osteoporotic effects.     

后生元(postbiotics):调节肝硬化患者肠道菌群及疾病进程的新策略

肝硬化是慢性肝炎发展的终末阶段,患者出现有不同程度的肠道菌群失调,并伴有肠道屏障功能的缺失和菌群移位,是引发肝硬化并发症的重要原因。尽管益生菌能在多个层面保护肠道屏障功能,但其在肝硬化肠道菌群紊乱中的疗效并不明确。现在的研究发现一些益生菌的组分或代谢产物有着与益生活菌类似的益生功效,包括稳定肠道菌群、加强肠上皮屏障功能和调节肠黏膜免疫反应等,其重要的优点是具有明确的分子结构和显著的生物活性,可能是未来调节肝硬化肠道菌群及疾病进程的新方向。本文主要总结了肝硬化肠道菌群失调对于肝硬化并发症及疾病进程的影响,探讨了益生菌的作用及局限性,并重点讨论后生元在调控肝硬化肠道菌群及疾病进程中的应用前景。     

后生元缓解胃肠道疾病的研究进展及其潜在机制

胃肠道是全身代谢最活跃的器官之一，也是人体内最大的细菌库。人体胃肠道中含有丰富的微生物群，其与宿主健康存在着错综复杂的关系。肠道菌群处于一种动态平衡的状态，当这种平衡被打破时会引起便秘、腹泻、肠易激综合征、炎症性肠病和结直肠癌等胃肠道疾病的发生。近年来，关于后生元的研究越来越多，其对肠道屏障的保护作用与益生菌类似甚至效果更佳。本文重点介绍了当前后生元在动物实验和临床中改善胃肠道疾病的相关研究，探讨了后生元在胃肠道中的作用及其在增强上皮屏障、调节免疫系统、肠道菌群和神经系统4个方面的潜在作用机制。