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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >Selective effects of Lactobacillus casei Shirota on T cell activation, natural killer cell activity and cytokine production.
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Selective effects of Lactobacillus casei Shirota on T cell activation, natural killer cell activity and cytokine production.

机译:干酪乳杆菌Shirota对T细胞活化,自然杀伤细胞活性和细胞因子产生的选择性作用。

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摘要

Modulation of host immunity is an important potential mechanism by which probiotics confer health benefits. This study was designed to investigate the effects of a probiotic strain, Lactobacillus casei Shirota (LcS), on immune function using human peripheral blood mononuclear cells (PBMC) in vitro. In addition, the role of monocytes in LcS-induced immunity was also explored. LcS promoted natural killer (NK) cell activity and preferentially induced expression of CD69 and CD25 on CD8(+) and CD56(+) subsets in the absence of any other stimulus. LcS also induced production of interleukin (IL)-1beta, IL-6, tumour necrosis factor (TNF)-alpha, IL-12 and IL-10 in the absence of lipopolysaccharide (LPS). In the presence of LPS, LcS enhanced IL-1beta production but inhibited LPS-induced IL-10 and IL-6 production, and had no further effect on TNF-alpha and IL-12 production. Monocyte depletion reduced significantly the impact of LcS on lymphocyte activation, cytokine production and natural killer (NK) cell activity. In conclusion, LcS activated cytotoxic lymphocytes preferentially in both the innate and specific immune systems, which suggests that LcS could potentiate the destruction of infected cells in the body. LcS also induced both proinflammatory and anti-inflammatory cytokine production in the absence of LPS, but in some cases inhibited LPS-induced cytokine production. Monocytes play an important role in LcS-induced immunological responses.
机译:调节宿主免疫力是益生菌赋予健康益处的重要潜在机制。这项研究旨在调查益生菌菌株干酪乳杆菌Shirota(LcS)对人外周血单个核细胞(PBMC)免疫功能的影响。此外,还探讨了单核细胞在LcS诱导的免疫中的作用。 LcS促进自然杀伤(NK)细胞活性,并在没有任何其他刺激的情况下,优先诱导CD8(+)和CD56(+)子集上CD69和CD25的表达。在不存在脂多糖(LPS)的情况下,LcS还诱导白介素(IL)-1beta,IL-6,肿瘤坏死因子(TNF)-α,IL-12和IL-10的产生。在LPS存在下,LcS增强了IL-1beta的产生,但抑制了LPS诱导的IL-10和IL-6的产生,并且对TNF-α和IL-12的产生没有进一步的影响。单核细胞耗竭显着降低了LcS对淋巴细胞活化,细胞因子产生和自然杀伤(NK)细胞活性的影响。总之,LcS在先天免疫系统和特异性免疫系统中均优先激活细胞毒性淋巴细胞,这表明LcS可以增强体内感染细胞的破坏。在不存在LPS的情况下,LcS还可诱导促炎和抗炎细胞因子的产生,但在某些情况下,会抑制LPS诱导的细胞因子的产生。单核细胞在LcS诱导的免疫反应中起重要作用。

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