Li Ai-Li, Sun Yi-Qio, Du Peng, Meng Xiang-Chen, Guo Ling, Li Shuang, Zhang Chao
Key laboratory of Dairy Science, Ministry of Education, College of Food Sciences, Northeast Agriculture University, Xiangfang District, Harbin, Heilongjiang, China.
Iran J Allergy Asthma Immunol. 2017 Apr;16(2):147-158.
Our previous study reported that Lactobacillus acidophilus(L.acidophilus) key laboratory of dairy science (KLDS) 1.0738 had an effective impact on inhibiting β-lactoglobulin (β-lg) allergy. This study further investigated the anti-allergic activity of peptidoglycan (PGN) isolated from KLDS 1.0738. This study aimed to assess whether toll-like receptor 2 (TLR2)/NF-kappaB (NF-κB) signaling activated by PGN was responsible for reducing allergic inflammation. Our data showed that administration of L. acidophilus PGN inhibited IgE production and improved the Treg/Th17 balance toward a Treg response in a mouse model of β-lg allergy. In addition, treating different doses L. acidophilus PGN to sensitized mice significantly increased TLR2 levels, along with enhancing NF-κB expression, especially in medium and high concentration (p<0.05). Further analysis revealed that the mRNA expression of TLR2 and NF-κB were positively correlated with the Foxp3 mRNA expression (p<0.05), but were negatively correlated with the RORγt mRNA expression in L. acidophilus PGN-treated group compared to allergy group (p<0.05). This study suggests PGN was similar to probiotics in preventing β-lg allergy through regulating Treg/Th17 imbalance, and activation of TLR2/NF-κB signaling may be involved in this process.
我们之前的研究报道,嗜酸乳杆菌(L. acidophilus)乳业科学重点实验室(KLDS)1.0738对抑制β-乳球蛋白(β-lg)过敏具有显著作用。本研究进一步探究了从KLDS 1.0738中分离出的肽聚糖(PGN)的抗过敏活性。本研究旨在评估PGN激活的Toll样受体2(TLR2)/核因子κB(NF-κB)信号通路是否对减轻过敏炎症起作用。我们的数据表明,在β-lg过敏小鼠模型中,给予嗜酸乳杆菌PGN可抑制IgE产生,并使Treg/Th17平衡向Treg反应方向改善。此外,用不同剂量的嗜酸乳杆菌PGN处理致敏小鼠,可显著提高TLR2水平,同时增强NF-κB表达,尤其是在中高浓度时(p<0.05)。进一步分析显示,与过敏组相比,嗜酸乳杆菌PGN处理组中TLR2和NF-κB的mRNA表达与Foxp3 mRNA表达呈正相关(p<0.05),但与RORγt mRNA表达呈负相关(p<0.05)。本研究表明,PGN在预防β-lg过敏方面与益生菌相似,可通过调节Treg/Th17失衡发挥作用,且TLR2/NF-κB信号通路的激活可能参与了这一过程。