Department of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
FEMS Microbiol Lett. 2010 Jan;302(2):189-96. doi: 10.1111/j.1574-6968.2009.01853.x. Epub 2009 Nov 13.
To study the mechanism of action of the lactobacilli, splenocytes were incubated with lactobacilli. We compared the ability of live and lyophilized Lactobacillus casei, Lactobacillus rhamnosus GG and Lactobacillus delbrueckii ssp. bulgaricus to modulate the production of interleukin 12p40 (IL-12p40), tumor necrosis factor alpha and IL-10 by splenocytes from C57BL/6 and BALB/c mice. Blocking contact between lactobacilli and immune cells abrogated all cytokine production. Toll-like receptor 2 (TLR2) was partially responsible, but not TLR4 or TLR9, for the induction of cytokine production in splenocytes. All cytokine production declined to basal levels when bacterial phagocytosis was inhibited. This shows that lactobacilli stimulation of cytokine production in splenocytes requires the process of phagocytosis and engagement of TLR2, but not TLR4 or TLR9.
为了研究乳酸菌的作用机制,我们用乳酸菌孵育了脾细胞。我们比较了活菌和冻干的干酪乳杆菌、鼠李糖乳杆菌 GG 和德氏乳杆菌保加利亚亚种对 C57BL/6 和 BALB/c 小鼠脾细胞产生白细胞介素 12p40(IL-12p40)、肿瘤坏死因子 alpha 和 IL-10 的能力。阻断乳酸菌与免疫细胞的接触会消除所有细胞因子的产生。Toll 样受体 2(TLR2)部分负责,但 TLR4 或 TLR9 不负责,诱导脾细胞产生细胞因子。当细菌吞噬作用被抑制时,所有细胞因子的产生都下降到基础水平。这表明乳酸菌刺激脾细胞产生细胞因子需要吞噬作用和 TLR2 的参与,但不需要 TLR4 或 TLR9。