Ryu Seung-Hyun, Park Jong-Hyung, Choi Soo-Young, Jeon Hee-Yeon, Park Jin-Il, Kim Jun-Young, Ham Seung-Hoon, Choi Yang-Kyu
Department of Laboratory Animal Medicine, College of Veterinary Medicine, Konkuk University, Seoul 05029, Republic of Korea.
J Microbiol Biotechnol. 2016 Jul 28;26(7):1333-40. doi: 10.4014/jmb.1602.02004.
The main objective of this study was to investigate whether Lactobacillus rhamnosus GG (LGG) ameliorated the effects of Citrobactor rodentium infection in Toll-like receptor 2 (TLR2) knockout (KO) and TLR4 KO mice, as well as in wild-type C57BL/6 (B6) mice. TLR2 KO, TLR4 KO, and B6 mice were divided into three groups per each strain. Each group had an uninfected control group (n = 5), C. rodentium-infected group (n = 8), and LGG-pretreated C. rodentium-infected group (n = 8). The survival rate of B6 mice infected with C. rodentium was higher when pretreated with LGG. Pretreatment with LGG ameliorated C. rodentium-induced mucosal hyperplasia in B6 and TLR4 KO mice. However, in C-rodentium-infected TLR2 KO mice, mucosal hyperplasia persisted, regardless of pretreatment with LGG. In addition, LGG-pretreated B6 and TLR4 KO mice showed a decrease in spleen weight and downregulation of tumor necrosis factor alpha, interferon gamma, and monocyte chemotactic protein 1 mRNA expression compared with the non-pretreated group. In contrast, such changes were not observed in TLR2 KO mice, regardless of pretreatment with LGG. From the above results, we conclude that pretreatment with LGG ameliorates C. rodentium-induced colitis in B6 and TLR4 KO mice, but not in TLR2 KO mice. Therefore, LGG protects mice from C. rodentium-induced colitis in a TLR2-dependent manner.
本研究的主要目的是调查鼠李糖乳杆菌GG（LGG）是否能改善啮齿柠檬酸杆菌感染对Toll样受体2（TLR2）基因敲除（KO）小鼠、TLR4基因敲除小鼠以及野生型C57BL/6（B6）小鼠的影响。每个品系的TLR2基因敲除小鼠、TLR4基因敲除小鼠和B6小鼠均分为三组。每组均设有未感染对照组（n = 5）、啮齿柠檬酸杆菌感染组（n = 8）和LGG预处理的啮齿柠檬酸杆菌感染组（n = 8）。用LGG预处理后，感染啮齿柠檬酸杆菌的B6小鼠存活率更高。LGG预处理改善了B6小鼠和TLR4基因敲除小鼠中啮齿柠檬酸杆菌诱导的黏膜增生。然而，在感染啮齿柠檬酸杆菌的TLR2基因敲除小鼠中，无论是否用LGG预处理，黏膜增生都持续存在。此外，与未预处理组相比，LGG预处理的B6小鼠和TLR4基因敲除小鼠脾脏重量减轻，肿瘤坏死因子α、干扰素γ和单核细胞趋化蛋白1 mRNA表达下调。相比之下，无论是否用LGG预处理，TLR2基因敲除小鼠均未观察到此类变化。根据上述结果，我们得出结论，LGG预处理可改善B6小鼠和TLR4基因敲除小鼠中啮齿柠檬酸杆菌诱导的结肠炎，但不能改善TLR2基因敲除小鼠中的结肠炎。因此，LGG以TLR2依赖的方式保护小鼠免受啮齿柠檬酸杆菌诱导的结肠炎。
