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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Toll-like receptor 2 and nucleotide-binding oligomerization domain-2 play divergent roles in the recognition of gut-derived lactobacilli and bifidobacteria in dendritic cells.
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Toll-like receptor 2 and nucleotide-binding oligomerization domain-2 play divergent roles in the recognition of gut-derived lactobacilli and bifidobacteria in dendritic cells.

机译：Toll样受体2和核苷酸结合的寡聚域2在识别树突状细胞中肠源性乳酸杆菌和双歧杆菌中起着不同的作用。

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摘要

The gut microbiota is vital in the maintenance of homeostasis in the gut immune system. Its diversity and composition play major roles in relation to allergies and inflammatory bowel diseases, and administration of lactic acid bacteria (LAB), such as lactobacilli and bifidobacteria, has positive effects on these pathologies. However, the mechanisms behind the beneficial effects are largely unknown. Here we reveal divergent roles played by Toll-like receptor-2 (TLR2) and nucleotide-binding oligomerization domain-2 (NOD2) in dendritic cell (DC) recognition of LAB. Murine bone-marrow-derived DC lacking NOD2 produce higher levels of interleukin-10 (IL-10) and reduced levels of IL-12 and tumour necrosis factor-alpha (TNF-alpha) in response to LAB. This indicates that peptidoglycan is partly responsible for the T helper type 1 skewing effect of certain LAB. Dendritic cells that are TLR2-/- produce less IL-12 and TNF-alpha and more IL-10 in response to some strains of lactobacilli, while they produce more IL-12 and less IL-10 in response to bifidobacteria. The same tendency was found in human monocyte-derived DC. We have previously reported that the weak IL-12-inducing and TNF-alpha-inducing bifidobacteria inhibit the T helper type 1 skewing effect induced by strong immunostimulatory lactobacilli. Here we show that this immunoinhibitory effect of bifidobacteria is dependent on TLR2 and independent of NOD2. Moreover, independently of the cytokine pattern induced by intact LAB, cell wall fractions of all LAB, as well as synthetic lipoproteins possess immunoinhibitory capacities in both human and murine DC. These novel findings suggest that LAB act as immunoregulators through interaction of lipoprotein with TLR2 and as immunostimulators through interaction of peptidoglycan with NOD2.
机译：肠道菌群对于维持肠道免疫系统的体内平衡至关重要。它的多样性和组成在变态反应和炎症性肠病方面起着重要作用，而乳酸菌（乳酸菌和双歧杆菌）的施用对这些病理学具有积极作用。但是，产生有益作用的机制尚不清楚。在这里，我们揭示了Toll样受体2（TLR2）和核苷酸结合寡聚域2（NOD2）在树突状细胞（DC）对LAB的识别中所起的不同作用。缺少NOD2的小鼠骨髓来源的DC产生更高水平的白介素10（IL-10），降低IL-12和肿瘤坏死因子-α（TNF-α）的水平。这表明肽聚糖部分负责某些LAB的T型辅助1型偏斜作用。 TLR2-/-树突状细胞对某些乳酸杆菌菌株产生的IL-12和TNF-α较少，而IL-10较多，而对双歧杆菌产生的IL-12和IL-10较少。在人类单核细胞来源的DC中发现了相同的趋势。我们以前曾报道过，弱诱导IL-12和TNF-α诱导的双歧杆菌抑制强免疫刺激性乳杆菌诱导的T辅助1型偏斜效应。在这里，我们表明双歧杆菌的这种免疫抑制作用取决于TLR2，而与NOD2不相关。此外，与完整的LAB诱导的细胞因子模式无关，所有LAB的细胞壁部分以及合成脂蛋白在人和鼠DC中均具有免疫抑制能力。这些新发现表明，LAB通过脂蛋白与TLR2的相互作用充当免疫调节剂，并通过肽聚糖与NOD2的相互作用充当免疫刺激剂。

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