Li Jinze, Li Qiuke, Wu Qianhui, Gao Nan, Wang Zhihua, Yang Yang, Shan Anshan
Institute of Animal Nutrition, Northeast Agricultural University, Harbin, 150030, P. R. China.
J Anim Sci Biotechnol. 2023 Mar 6;14(1):23. doi: 10.1186/s40104-023-00830-7.
Salmonella typhimurium (S.T), as an important foodborne bacterial pathogen, can cause diarrhea and gastroenteritis in humans and animals. Numerous studies have confirmed that exopolysaccharides (EPSs) have various biological functions, but the mechanism through which EPSs improve the immunity of animals against the invasion of pathogenic bacteria is unclear. Here, we explored the protective effect of EPSs of Lactobacillus rhamnosus GG (LGG) on the S.T-infected intestine.
Mice received adequate food and drinking water for one week before the start of the experiment. After 7 d of prefeeding, 2×10 CFU/mL S.T solution and an equivalent volume of saline (control group) were given orally for 1 d. On the fourth day, the mice were treated with 0.5 mg/mL EPSs, 1.0 mg/mL EPSs, 2.0 mg/mL EPSs, or 2.0 mg/mL penicillin for 7 d. Finally, the body and relative organ weight, histological staining, and the levels of antioxidant enzyme activity and inflammatory cytokines were determined.
The S.T-infected mice exhibited symptoms of decreased appetite, somnolence, diarrhea and flagging spirit. Treatment with EPSs and penicillin improved the weight loss of the mice, and the high dose of EPSs showed the best therapeutic effect. EPSs significantly ameliorated S.T-induced ileal injury in mice. High-dose EPSs were more effective than penicillin for alleviating ileal oxidative damage induced by S.T. The mRNA levels of inflammatory cytokines in the ileum of mice showed that the regulatory effects of EPSs on inflammatory cytokines were better than those of penicillin. EPSs could inhibit the expression and activation of key proteins of the TLR4/NF-κB/MAPK pathway and thereby suppress the level of S.T-induced ileal inflammation.
EPSs attenuate S.T-induced immune responses by inhibiting the expression of key proteins in the TLR4/NF-κB/MAPK signaling pathway. Moreover, EPSs could promote bacterial aggregation into clusters, which may be a potential strategy for reducing the bacterial invasion of intestinal epithelial cells.
鼠伤寒沙门氏菌（S.T）作为一种重要的食源性细菌病原体，可导致人和动物腹泻及肠胃炎。众多研究证实胞外多糖（EPSs）具有多种生物学功能，但EPSs提高动物抵抗病原菌侵袭免疫力的机制尚不清楚。在此，我们探究了鼠李糖乳杆菌GG（LGG）的EPSs对S.T感染肠道的保护作用。
实验开始前一周，小鼠给予充足食物和饮用水。预喂7天后，口服2×10 CFU/mL S.T溶液和等体积生理盐水（对照组）1天。第四天，小鼠分别用0.5 mg/mL EPSs、1.0 mg/mL EPSs、2.0 mg/mL EPSs或2.0 mg/mL青霉素处理7天。最后，测定体重和相关器官重量、组织学染色以及抗氧化酶活性和炎性细胞因子水平。
S.T感染的小鼠表现出食欲下降、嗜睡、腹泻和精神萎靡的症状。用EPSs和青霉素处理可改善小鼠体重减轻情况，高剂量EPSs显示出最佳治疗效果。EPSs显著改善了S.T诱导的小鼠回肠损伤。高剂量EPSs在减轻S.T诱导的回肠氧化损伤方面比青霉素更有效。小鼠回肠中炎性细胞因子的mRNA水平表明，EPSs对炎性细胞因子的调节作用优于青霉素。EPSs可抑制TLR4/NF-κB/MAPK途径关键蛋白的表达和激活，从而抑制S.T诱导的回肠炎症水平。
EPSs通过抑制TLR4/NF-κB/MAPK信号通路中关键蛋白的表达来减轻S.T诱导的免疫反应。此外，EPSs可促进细菌聚集形成菌团，这可能是减少细菌侵袭肠上皮细胞的一种潜在策略。
