MyD88 but not TLR2, 4 or 9 is essential for IL-12 induction by lactic acid bacteria
MyD88 but not TLR2, 4 or 9 is essential for IL-12 induction by lactic acid bacteria
复制标题
DOI：
10.1271/bbb.70414
复制
发表时间：
2007-12-01
影响因子：
1.6
通讯作者：
Konishi, Yutaka
中科院分区：
文献类型：
--
作者：
Ichikawa, Shintaro;Fujii, Rei;Konishi, Yutaka
虽然乳酸菌（LAB）影响免疫系统，例如，具有抗过敏作用，但对免疫调节的实际机制知之甚少。Toll样受体（TLR）识别保守的微生物分子模式，并被推测参与LAB的识别。然而，很少有详细的报告检查TLR和LAB之间的关系。我们在这里测量了IL-12的产生，IL-12是一种被认为在抗过敏作用中起重要作用的细胞因子，由副干酪乳杆菌菌株KW 3110和其他典型的LAB通过来自TLR 2-、TLR 4-、TLR 9-和髓样分化因子88（MyD 88）缺陷型小鼠的细胞诱导。出乎意料的是，观察到野生型和TLR 2-、4-和9-缺陷小鼠的类似细胞因子产生。相比之下，MyD 88缺陷小鼠的细胞对LAB刺激没有反应。因此得出结论，尽管LAB，包括菌株KW 3110，不太可能被TLR 2、4或9识别，但MyD 88对于对这些细菌的应答是必需的。
Although lactic acid bacteria (LAB) affect the immune system, for example, having an anti-allergic effect, little is known about the actual mechanisms of immune modulation. Toll-like receptors (TLRs) recognize conserved microbial molecular patterns, and are presumed to be involved in the recognition of LAB. However, there are few detailed reports examining the relationships between TLR and LAB. We measured here production of IL-12, a cytokine considered to play an important role in anti-allergic effects, induced by Lactobacillus paracasei strain KW3110 and other typical LAB by cells from TLR2-, TLR4-, TLR9- and myeloid differentiation factor 88 (MyD88)-deficient mice. Unexpectedly, similar cytokine production from wild-type and TLR2-, 4- and 9-deficient mice was observed. In contrast, cells from MyD88-deficient mice failed to respond to stimulation with LAB. It is therefore concluded that although LAB, including strain KW3110, are not likely to be recognized by TLR2, 4 or 9, MyD88 is essential for the response to these bacteria.