Zhao Chenpei, Chen Huan, Liang Hao, Zhao Xiaoyu, Tang Wenli, Wei Maolian, Li Youzhi, Zhang Jianlong, Yu Xin, Chen Guozhong, Zhu Hongwei, Jiang Linlin, Zhang Xingxiao
School of Life Sciences, Ludong University, Yantai, China.
Department of Microbiology, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, China.
Front Pharmacol. 2022 Mar 7;13:832245. doi: 10.3389/fphar.2022.832245. eCollection 2022.
can interact with macrophages against bacterial enteropathy due to its potential ability to modulate macrophage polarization. However, this mechanism is not completely understood. TLR2 can recognize microbial components and trigger macrophage cytokine responses to different gram-positive strains. The aim of this study was to investigate whether probiotic RS-09 can induce macrophage polarization against Typhimurium infection via TLR2 signalling. BALB/c mice were preadministered RS-09 continuously for 7 days and then infected with Typhimurium ATCC14028. Mouse RAW264.7 mononuclear macrophages were stimulated with RS-09 and coincubated with ATCC14028 or PBS controls. The results of the study indicated that RS-09 could relieve . Typhimurium-induced splenomegaly, body weight loss and death rate. RS-09 also limited the colonization and translocation of . Typhimurium in the gastrointestinal tract and thereby protected against infection. We also observed that RS-09 upregulated the production of M1 macrophage characteristics (e.g., CD11c and IL-6) against . Typhimurium. Furthermore, RS-09 induced the expression of TLR2 in macrophages. In an study, treatment of RAW264.7 cells with RS-09 either concurrently with or before . Typhimurium challenge enhanced the secretion of Reactive oxygen species and Nitric oxide. This effect was related to TLR2 and NF-κB activation. Based on these findings, RS-09 was shown to modulate M1 macrophage polarization and induce TLR2-linked NF-κB signalling activity in the innate immune response to . Typhimurium infection.
由于其调节巨噬细胞极化的潜在能力,它可以与巨噬细胞相互作用以对抗细菌性肠病。然而,这种机制尚未完全被理解。TLR2可以识别微生物成分并触发巨噬细胞对不同革兰氏阳性菌株的细胞因子反应。本研究的目的是调查益生菌RS-09是否能通过TLR2信号通路诱导巨噬细胞极化以抵抗鼠伤寒沙门氏菌感染。将BALB/c小鼠连续7天预先给予RS-09,然后感染鼠伤寒沙门氏菌ATCC14028。用RS-09刺激小鼠RAW264.7单核巨噬细胞,并与ATCC14028或PBS对照共同孵育。研究结果表明,RS-09可以缓解鼠伤寒沙门氏菌诱导的脾肿大、体重减轻和死亡率。RS-09还限制了鼠伤寒沙门氏菌在胃肠道中的定植和移位,从而预防感染。我们还观察到,RS-09上调了针对鼠伤寒沙门氏菌的M1巨噬细胞特征(如CD11c和IL-6)的产生。此外,RS-09诱导巨噬细胞中TLR2的表达。在一项研究中,在鼠伤寒沙门氏菌攻击前或同时用RS-09处理RAW264.7细胞可增强活性氧和一氧化氮的分泌。这种效应与TLR2和NF-κB的激活有关。基于这些发现,RS-09在对鼠伤寒沙门氏菌感染的先天免疫反应中被证明可调节M1巨噬细胞极化并诱导与TLR2相关的NF-κB信号活性。