Bhatia Ruchika, Sharma Shikha, Bhadada Sanjay Kumar, Bishnoi Mahendra, Kondepudi Kanthi Kiran
Healthy Gut Research Group, Centre for Excellence in Functional Foods, Food and Nutrition Biotechnology Division, National Agri-Food Biotechnology Institute, Sahibzada Ajit Singh Nagar, India.
Department of Biotechnology, Panjab University, Chandigarh, India.
Front Microbiol. 2022 Jun 13;13:930928. doi: 10.3389/fmicb.2022.930928. eCollection 2022.
Lipopolysaccharide (LPS), a gut-transmitted endotoxin from Gram-negative bacteria, causes inflammatory diseases leading to the loss of gut barrier integrity and has been identified as a major pathogenic stimulator in many dysfunctions. Hence, supplementation with probiotics is believed to be one of the most effective strategies for treating many inflammatory gut disorders. Although probiotics are known to have a variety of therapeutic characteristics and to play a beneficial role in host defense responses, the molecular mechanisms by which they achieve these beneficial effects are unknown due to species- and strain-specific behaviors. Therefore, in this study, the protective role of five indigenous lactic acid bacterial strains in ameliorating LPS-induced gut barrier impairment in the C57BL/6 mice model was elucidated. LAB3, LAB20, and LAB31 were isolated from infant feces; LAB8 from fermented food (Bekang); and LAB39 from beetroot. Intraperitoneal injection of LPS (10 mg/kg of body weight) increased the levels of lipocalin and serum markers TNF-α, IL-6, and IL-1β, and the overall disease activity index in the treated group. Furthermore, gene expression of , , and ; mucin-producing genes and ; and intestinal alkaline phosphatase (IAP) was deleteriously altered in the ileum of LPS-treated mice. Furthermore, LPS also induced dysbiosis in gut microbiota where higher abundances of , , and and decreased abundances of , , , and were observed. Western blotting results also suggested that LPS treatment causes the loss of gut barrier integrity relative to the pre-supplementation with LAB strains, which enhanced the expression of tight junction proteins and ameliorated the LPS-induced changes and inflammation. Taken together, the study suggested that LAB3 and LAB39 were more potent in ameliorating LPS-induced gut inflammation and dysbiosis.
脂多糖（LPS）是一种来自革兰氏阴性菌的肠道传播内毒素，可引发炎症性疾病，导致肠道屏障完整性丧失，并且已被确认为许多功能障碍中的主要致病刺激因素。因此，补充益生菌被认为是治疗多种炎症性肠道疾病的最有效策略之一。尽管已知益生菌具有多种治疗特性并在宿主防御反应中发挥有益作用，但由于其物种和菌株特异性行为，它们实现这些有益效果的分子机制尚不清楚。因此，在本研究中，阐明了五种本土乳酸菌菌株在改善C57BL/6小鼠模型中LPS诱导的肠道屏障损伤方面的保护作用。LAB3、LAB20和LAB31从婴儿粪便中分离得到；LAB8从发酵食品（贝康）中分离得到；LAB39从甜菜根中分离得到。腹腔注射LPS（10mg/kg体重）会增加治疗组中脂质运载蛋白水平以及血清标志物TNF-α、IL-6和IL-1β水平，还有整体疾病活动指数。此外，LPS处理小鼠的回肠中，、和的基因表达；产生粘蛋白的基因和；以及肠碱性磷酸酶（IAP）发生了有害改变。此外，LPS还诱导了肠道微生物群的失调，观察到、和的丰度较高，而、、和的丰度降低。蛋白质印迹结果还表明，与预先补充LAB菌株相比，LPS处理会导致肠道屏障完整性丧失，预先补充LAB菌株可增强紧密连接蛋白的表达，并改善LPS诱导的变化和炎症。综上所述，该研究表明LAB3和LAB39在改善LPS诱导的肠道炎症和失调方面更有效。
