Hyperuricemia is a metabolic disease caused by disturbances in purine metabolism and imbalances in the formation and excretion of uric acid. It is closely related to the gut microbiota, which is considered a therapeutic target. Some lactic acid bacteria with a uric acid lowering effect have the potential to ameliorate hyperuricemia in the host. However, the mechanism of action remains unclear. Here, we screened a strain of Lactobacillus acidophilus F02 that efficiently degrades uric acid precursors (inosine and guanosine) and further investigated its underlying mechanism on the alleviation of hyperuricemia in high fructose-adenine induced mice. Results showed that L. acidophilus F02 administration reduced serum uric acid levels in hyperuricemia mice by inhibiting xanthine oxidase and adenosine deaminase activity, while protecting hepatorenal injury and systemic inflammation by regulating the relative expression of NLRP3 inflammasome. Most importantly, it restored gut microbial homeostasis and the abundance of bacterial taxa (i.e., a balance in the relative abundance of Firmicutes and Actinobacteria and an increase in the abundance of Bacteroides, Ruminococcus and Lactobacillus). Furthermore, the ability of L. acidophilus F02 to lower uric acid and suppress NLRP3 inflammasome expression was confirmed in the HK-2 cell model, as well as the multiple immunomodulatory effects on RAW264.7 cells. Taken together, we speculate that fructose-adenine induced hyperuricemia triggers hepatorenal injury and gut microbiota dysbiosis, which is ameliorated by L. acidophilus F02. Collectively, the results suggest that lowering uric acid synthesis, increasing uric acid excretion and reducing NLRP3-related IL-1β levels are effective strategies to ameliorate hyperuricemia. Such information could inform future studies on the ecology of L. acidophilus and guide the use of this species for dietary applications in the food industry.

Hyperuricemia is a metabolic disease with excessively high level of uric acid in blood. It is triggered by the disorder of purine metabolism and/or uric acid excretion in human, and the purine-rich and fructose-rich diets and purine was confirmed to induce the hyperuricemia. In recent years, some reports have shown that there is a close connection between hyperuricemia and gut microbiota, namely the patients with hyperuricemia have a gut microbiota disorder and decreased abundance of beneficial bacteria. Rational diet and probiotics intake have been confirmed to regulate intestinal microbiota effectively, maintain homeostasis, and promote intestinal purine and uric acid metabolism. Thus, gut microbiota is considered as a target for future preventation of hyperuricemia. In the review, we summarized the feature and pathogenesis of hyperuricemia, the induction of diet on hyperuricemia, the association between hyperuricemia and gut microbiota, and the regulation strategies of gut microbiota on hyperuricemia. This review will provide reference for the diagnosis and treatment of hyperuricemia and gout in the future.

为探究功能低聚糖对植物乳杆菌ZDY2013发酵乳的发酵特点和冷藏期功能的影响,选取具有益生元特性的低聚木糖、低聚异麦芽糖及其组合物为发酵乳中碳水化合物,评价发酵乳中植物乳杆菌发酵特性和pH值变化,同时对发酵乳的持水性及冷藏期抗氧化活性进行解析.结果表明:植物乳杆菌能利用不同浓度功能低聚糖进行代谢;相比葡萄糖,发酵乳中添加低聚糖更有利于植物乳杆菌的生长,尤其是其组合物浓度为3.0％时,能显著提高发酵乳中活菌数及降低发酵乳pH值;冷藏期(21 d)内,各组发酵乳活菌数呈下降趋势,但均高于108 cfu/g,pH值在7 d后比较稳定,而持水性不断增强;发酵乳DPPH自由基清除能力在第7 d最强,而ABTS+和羟自由基的清除能力呈下降趋势,且添加同浓度的组合物优于葡萄糖.该研究结果将为功能低聚糖及植物乳杆菌ZDY2013在乳品开发中的应用提供理论依据.

依据菌株宿主适应性特点,从健康家禽新鲜粪便中定向筛选具有开发潜力的罗伊氏乳杆菌.经16S rDNA序列分析和pduC基因筛查,获得3株产抗菌物质Reuterin的罗伊氏乳杆菌,对其耐受模拟胃肠道环境、抗生素敏感性、甘油发酵上清液抑菌活性及肠上皮细胞黏附能力等生物学特性进行系统评价.结果 表明,罗伊氏乳杆菌WLRE01、WLRE03、WLRE04均具有较强耐受极端酸(pH 2.5和pH 3.5)、胆盐(1.5 g/L)及模拟胃肠液的能力;经1 mmol/L过氧化氢处理6h,WLRE03、WLRE04的活菌数能基本维持初始浓度;甘油发酵上清液对金黄色葡萄球菌具有极强的抑制作用,抑菌圈最高达(28.1±1.2) mm;3株菌对HT-29细胞均具有良好的黏附特性,其中WLRE01黏附能力最强.综上所述,健康家禽肠道源的3株产Reuterin的罗伊氏乳杆菌可作为益生菌候选菌株进行深入研究.