Olaya Galán N N, Ulloa Rubiano J C, Velez Reyes F A, Fernandez Duarte K P, Salas Cárdenas S P, Gutierrez Fernandez M F
Laboratorio de Virología, Grupo de Enfermedades Infecciosas, Departamento de Microbiología, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, Colombia.
Departamento de Matemáticas, Facultad de Ciencias, Universidad El Bosque, Bogotá, Colombia.
J Appl Microbiol. 2016 Apr;120(4):1041-51. doi: 10.1111/jam.13069.
The aim of this study was to determine the antiviral activity of four probiotic metabolites (Lactobacillus and Bifidobacetrium species) against rotavirus in vitro infection monitored by the NSP4 protein production and Ca(2+) release.
The antiviral effect of the metabolites was performed due a comparison between a blocking model and an intracelullar model on MA104 cells, with the response of NSP4 production and Ca(2+) liberation measured by flow cytometry. Significant results were obtained with the metabolites of Lactobacillus casei, and Bifidobacterium adolescentis in the reduction of the protein production (P = 0·04 and P = 0·014) and Ca(2+) liberation (P = 0·094 and P = 0·020) in the intracellular model, which suggests a successful antiviral activity against RV infection.
This study demonstrates that probiotic metabolites were able to interfere with the final amount of intracellular NSP4 protein and a successful Ca(2+) regulation, which suggests a new approach to the mechanism exerted by probiotics against the rotavirus infection.
A novel anti-rotaviral effect exerted by probiotic metabolites monitored by the NSP4 protein during the RV in vitro infection and the effect on the Ca(2+) release is reported; suggesting a reduction on the impact of the infection by decreasing the damage of the cells preventing the electrolyte loss.
本研究旨在通过监测NSP4蛋白产生和Ca(2+)释放,确定四种益生菌代谢产物(乳酸杆菌和双歧杆菌属)对轮状病毒体外感染的抗病毒活性。
通过比较阻断模型和细胞内模型对MA104细胞的作用来评估代谢产物的抗病毒效果,采用流式细胞术测量NSP4产生和Ca(2+)释放的反应。干酪乳杆菌和青春双歧杆菌的代谢产物在细胞内模型中显著降低了蛋白产生(P = 0·04和P = 0·014)和Ca(2+)释放(P = 0·094和P = 0·020),这表明对轮状病毒感染具有成功的抗病毒活性。
本研究表明益生菌代谢产物能够干扰细胞内NSP4蛋白的最终量并成功调节Ca(2+),这提示了益生菌对抗轮状病毒感染机制的新方法。
报道了在轮状病毒体外感染期间,益生菌代谢产物通过NSP4蛋白监测到的新型抗轮状病毒作用及其对Ca(2+)释放的影响;表明通过减少细胞损伤和防止电解质流失来降低感染的影响。