Bifidobacterium bifidum alleviates adenine-induced acute kidney injury in mice by improving intestinal barrier function.

Acute kidney injury (AKI) is a kind of critical kidney disease characterized by tubular injury, rapid decline of renal function and renal inflammation, with high clinical incidence. AKI has been shown to be associated with dysregulation of the gut microbiota and impaired intestinal barrier. Bifidobacterium has a positive impact on the treatment of many diseases. However, little is known about the role and mechanism of Bifidobacterium in AKI. Based on previous experiments, Bifidobacterium bifidum FL228.1 and FL276.1, which can relieve intestinal inflammation, and Bifidobacterium bifidum ZL.1, which has anti-inflammatory potential, were screened. This study aimed to investigate the effects of Bifidobacterium bifidum FL228.1, FL276.1 and ZL.1 on AKI, focusing on their role in the gut microbiota composition and intestinal barrier function. Our results showed that Bifidobacterium bifidum FL228.1, FL276.1 and ZL.1 effectively improved kidney function in mice with AKI by regulating the gut microbiota dysregulation, inhibiting intestinal inflammation and rebuilding the intestinal mucosal barrier. In addition, intervention with probiotics turned the gut microbiota disturbance caused by AKI into a normalized trend, reversed the adverse outcome of microbiota imbalance, and increased the abundance of potentially beneficial bacteria Bifidobacterium and Faecalibaculum. In summary, Bifidobacterium bifidum FL228.1, FL276.1, and ZL.1 alleviate adenine-induced AKI based on the gut-kidney axis. Although their mechanisms of action are different, their effect on alleviating AKI is almost the same.

Probiotics induce intestinal IgA secretion in weanling mice potentially through promoting intestinal APRIL expression and modulating the gut microbiota composition.

Intestinal infections are strongly associated with infant mortality, and intestinal immunoglobulin A (IgA) is important to protect infants from intestinal infections after weaning. This study aims to screen probiotics that can promote the production of intestinal IgA after weaning and further explore their potential mechanisms of action. In this study, probiotics promoting intestinal IgA production were screened in weanling mouse models. The results showed that oral administration of Bifidobacterium bifidum (B. bifidum) FL228.1 and Bifidobacterium bifidum (B. bifidum) FL276.1 significantly enhanced IgA levels in the small intestine and upregulated the expression of a proliferation-inducing ligand (APRIL) and its upstream regulatory factor toll-like receptor 4 (TLR4). Furthermore, B. bifidum FL228.1 upregulated the relative abundance of Lactobacillus, while B. bifidum FL276.1 increased the relative abundance of Marvinbryantia and decreased Mucispirillum, further elevating intestinal IgA levels. In summary, B. bifidum FL228.1 and B. bifidum FL276.1 can induce IgA production in the intestinal tract of weanling mice by promoting intestinal APRIL expression and mediating changes in the gut microbiota, thus playing a significant role in enhancing local intestinal immunity in infants.

Bifidobacterium improves oestrogen-deficiency-induced osteoporosis in mice by modulating intestinal immunity.

Osteoporosis has become one of the major diseases that threaten the health of middle-aged and elderly people, and with the growth of an ageing population, more and more people are affected by osteoporosis these days. In recent years, intestinal flora has been found to affect the host immune system, and an overactive immune system is closely related to bone resorption. Probiotics can effectively improve bone density and strength, reduce bone loss, and improve osteoporosis, but their mechanism of action and relationship with intestinal microbiota are still unclear. In this study, two strains of Bifidobacterium (Bifidobacterium bifidum FL228.1 and Bifidobacterium animalis subsp. Lactis F1-7) that can alleviate intestinal inflammation were screened based on previous experiments. Through the construction of an ovariectomized mouse model, the improvement of osteoporosis by Bifidobacterium was detected, and the influence of Bifidobacterium on intestinal immunity was explored. The results show that Bifidobacterium treatment significantly improved bone mineral density (BMD), bone volume/total volume ratio (BV/TV), and trabecular number (Tb·N), and effectively suppressed bone loss. Furthermore, Bifidobacterium treatment could inhibit the expression of inflammatory cytokines in the gut, alleviate gut inflammation, and thus suppress excessive osteoclast generation. Its mechanism of action includes factors that protect the mucosal barrier, including occludin, ZO-1, claudin-2, and MUC2, and the reduction of pro-inflammatory M1 macrophages. B. bifidum FL228.1 increased the abundance of beneficial bacteria in the colon, including Lactobacillus and Colidextribacter. B. animalis F1-7 increased the abundance of Bifidobacterium and decreased the abundance of Desulfovibrio and Ruminococcus in the colon. These research findings expand our understanding of the gut-bone axis and provide new guidance for the development of probiotic-based therapies for osteoporosis in the future.

Krill Oil Combined with Bifidobacterium animalis subsp. lactis F1-7 Alleviates the Atherosclerosis of ApoE-/- Mice.

There has been an increasing number of studies on the interaction between active substances and probiotics to improve disease. Both krill oil (KO) and probiotics have the effect of improving atherosclerotic cardiovascular disease, but the combined effect has not been explored. Therefore, the purpose of this study was to explore the improvement effect of KO combined with probiotics on atherosclerosis. The atherosclerotic plaque area of ApoE-/- mice was detected after the intervention of KO, Bifidobacterium animalis subsp. lactis F1-7 (Bif. animalis F1-7), and KO combined with Bif. animalis F1-7. The results showed that Bif. animalis F1-7, KO, and KO combined with Bif. animalis F1-7 could significantly reduce the area of atherosclerotic plaque and improve the levels of serum lipids and inflammatory factors. They could regulate the farnesoid X receptor (FXR)/cholesterol 7-alpha hydroxylase (CYP7A1) pathway to reduce lipid accumulation. The intervention groups could also improve the inflammatory response by downregulating the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88) pathway. The anti-inflammatory effect of the interaction group was significantly better than that of KO. It proved that Bif. animalis F1-7 might play a synergistic effect in the improvement of inflammation by KO to the alleviation of atherosclerosis.