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.

中文翻译：

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独特的益生菌特征在肠上皮细胞中具有共同的 TLR2 依赖性信号传导。

益生菌和后生元的潜在机制尚不清楚，但众所周知，两者都会影响适应性和先天性免疫反应。此外，越来越多的人认为某些益生菌菌株具有提供某些健康益处的共同核心机制。在这里，我们旨在阐明益生菌菌株副加氏乳杆菌K7、发酵脂肪乳杆菌L930BB、动物双歧杆菌亚种的信号传导。动物IM386 和植物乳杆菌WCFS1。我们在体外实验中表明，所测试的益生菌表现出常见的 TLR2 和 TLR10 依赖性下游信号级联反应，涉及抑制 NF-κB 信号转导。在炎症条件下，益生菌激活磷脂酰肌醇 3-激酶 (PI3K)/Akt 抗凋亡通路和蛋白激酶 C (PKC) 依赖通路，从而调节肌动蛋白细胞骨架和紧密连接。这些途径有助于肠上皮细胞的再生和粘膜免疫系统的调节，这与经典 TLR 信号传导的抑制一起，促进了一般的免疫耐受。通过这项研究，我们确定了共享的益生菌机制，并且是第一个通过 TLR10 确定抗炎益生菌信号传导作用的人。