Protective effect of plantaricin bio-LP1 bacteriocin on multidrug-resistance Escherichia Coli infection by alleviate the inflammation and modulate of gut-microbiota in BALB/c mice model

微生物学 抗生素 多重耐药 促炎细胞因子 生物 大肠杆菌 肠道菌群 免疫系统 炎症 免疫学 生物化学 基因
作者
Mohamedelfatieh Ismael,Nageena Qayyum,Yaxin Gu,Yu Zhezhe,Yanlong Cui,Yu Zhang,Xin Lü
出处
期刊:International Journal of Biological Macromolecules [Elsevier]
卷期号:246: 125700-125700 被引量:7
标识
DOI:10.1016/j.ijbiomac.2023.125700
摘要

The rapid spread of multidrug-resistant pathogens with the low efficacy of common antibiotics for humans and animals in its clinical therapeutics are a global health concern. Therefore, there is a need to develop new treatment strategies to control them clinically. The study aimed to evaluate the effects of Plantaricin Bio-LP1 bacteriocin produced from Lactiplantibacillus plantarum NWAFU-BIO-BS29 to alleviate the inflammation caused by multidrug-resistance Escherichia Coli (MDR-E. coli) infection in BALB/c mice-model. The focus was given on aspects linked to the mechanism of the immune response. Results indicated that Bio-LP1 had highly promising effects on partially ameliorating MDR-E. coli infection by reducing the inflammatory response through inhibiting the overexpression of proinflammatory-cytokines such as secretion of tumor necrosis factor (TNF-α) and interleukin (IL-6 and IL-β) and strongly regulated theTLR4 signaling-pathway. Additionally, avoided the villous destruct, colon length shortening, loss of intestinal barrier integrity, and increased disease activity index. Furthermore, significantly increased the relative abundance of beneficial-intestinal-bacteria including Ligilactobacillus, Enterorhabdus, Pervotellaceae, etc. Finally, improved the intestinal mucosal barrier to alleviate the pathological damages and promote the production of short-chain fatty acids (SCFAs) a source of energy for the proliferation. In conclusion, plantaricin Bio-LP1 bacteriocin can be considered a safe alternative to antibiotics against MDR-E. coli-induced intestinal inflammation.
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