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Isolation and Characterization of Potentially Probiotic Bacterial Strains from Mice: Proof of Concept for Personalized Probiotics

机译:小鼠潜在益生菌菌株的分离和表征:个性化益生菌的概念证明

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摘要

Modulation of the gut microbiota through the use of probiotics has been widely used to treat or prevent several intestinal diseases. However, inconsistent results have compromised the efficacy of this approach, especially in severe conditions such as inflammatory bowel disease (IBD). The purpose of our study was to develop a personalized probiotic strategy and assess its efficacy in a murine model of intestinal inflammation. Commensal bacterial strains were isolated from the feces of healthy mice and then administered back to the host as a personalized treatment in dextran sodium sulfate (DSS)-induced colitis. Colonic tissues were collected for histological analysis and to investigate inflammatory markers such as Il-1β, Il-6, TGF-β, and Il-10, and the enzyme myeloperoxidase as a neutrophil marker. The group that received the personalized probiotic showed reduced susceptibility to DSS-colitis as compared to a commercial probiotic. This protection was characterized by a lower disease activity index and reduced histopathological damage in the colon. Moreover, the personalized probiotic was more effective in modulating the host immune response, leading to decreased Il-1β and Il-6 and increased TGF-β and Il-10 expression. In conclusion, our study suggests that personalized probiotics may possess an advantage over commercial probiotics in treating dysbiotic-related conditions, possibly because they are derived directly from the host’s own microbiota.
机译:通过使用益生菌来调节肠道微生物群已广泛用于治疗或预防几种肠道疾病。但是,不一致的结果损害了该方法的有效性,特别是在诸如炎症性肠病(IBD)等严重疾病中。我们研究的目的是开发个性化的益生菌策略并评估其在小鼠肠道炎症模型中的功效。从健康小鼠的粪便中分离出共生细菌菌株,然后作为葡聚糖硫酸钠(DSS)诱导的结肠炎的个性化治疗,再次施用于宿主。收集结肠组织用于组织学分析并研究炎性标志物,例如II-1β,II-6,TGF-β和II-10,以及髓过氧化物酶作为中性粒细胞标志物。与商业益生菌相比,接受个性化益生菌的人群对DSS结肠炎的敏感性降低。这种保护的特征在于较低的疾病活动指数和减少的结肠组织病理学损害。而且,个性化的益生菌在调节宿主免疫应答中更有效,导致II-1β和II-6减少以及TGF-β和II-10表达增加。总之,我们的研究表明,个性化益生菌在治疗与益生菌有关的疾病方面可能比商业益生菌更具优势,这可能是因为它们直接来源于宿主自身的微生物群。

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