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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。

Selective effects of Lactobacillus casei Shirota on T cell activation, natural killer cell activity and cytokine production.

机构信息

Department of Food and Nutritional Sciences, University of Reading, Reading, UK.

出版信息

Clin Exp Immunol. 2010 Aug;161(2):378-88. doi: 10.1111/j.1365-2249.2010.04173.x. Epub 2010 May 7.

Abstract

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.

摘要

宿主免疫调节是益生菌发挥健康益处的一个重要潜在机制。本研究旨在使用体外人外周血单核细胞(PBMC)研究益生菌菌株干酪乳杆菌 Shirota(LcS)对免疫功能的影响。此外,还探讨了单核细胞在 LcS 诱导免疫中的作用。LcS 促进自然杀伤(NK)细胞活性,并在没有其他刺激物的情况下优先诱导 CD8(+)和 CD56(+)亚群上的 CD69 和 CD25 的表达。LcS 还诱导白细胞介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α、IL-12 和 IL-10 的产生,而无需脂多糖(LPS)。在 LPS 存在的情况下,LcS 增强了 IL-1β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。单核细胞耗竭显著降低了 LcS 对淋巴细胞活化、细胞因子产生和 NK 细胞活性的影响。总之,LcS 优先在固有和特异性免疫系统中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。LcS 还在没有 LPS 的情况下诱导促炎和抗炎细胞因子的产生,但在某些情况下抑制 LPS 诱导的细胞因子产生。单核细胞在 LcS 诱导的免疫反应中发挥重要作用。

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