Wecare Probiotics Co., Ltd.

Probiotics play a crucial role in modulating the immune system and maintaining intestinal epithelial barrier integrity. The study investigates the effects of high-activity probiotic yogurt on immunosuppressed mice induced by cyclophosphamide (CTX). ICR male mice (8-week-old) were injected intraperitoneally with CTX (80 mg/kg body weight/day) on days 7, 8, and 9 to establish an immunosuppressive model (n = 10). Mice were fed a normal diet or high-activity probiotic yogurt for consecutive 14 days. The effect of three high-activity probiotic yogurt(10⁹ CFU/250 g, 10¹⁰ CFU/250 g, and 10¹¹ CFU/250 g, named as LPY, MPY, and HPY) on immunosuppressed mice was investigated by HE staining, enzyme-linked immunosorbent assay (ELISA), Western blotting, and 16 s rRNA sequencing. Results indicated that high-activity probiotic yogurt significantly increased the immune organ indices, interleukin-6 (IL-6), interleukin-12p70 (IL-12p70), tumor necrosis factor-α (TNF-α), and improved intestinal structure (P < 0.05). Western blotting revealed that high-activity probiotic yogurt improves the expression of toll-like receptor 4 (TLR4), nuclear factor kappa-B-p65 (p65), and TNF receptor associated factor 6 (TRAF6). Furthermore, 16 s rRNA analysis demonstrated that high-activity probiotic yogurt increased the diversity and richness of the gut microbiota, and the effect of LPY performed better than MPY and HPY. These findings indicated that high-activity probiotic yogurt may improve the immune function of mice by improving intestinal homeostasis and activation of the TLR4/NF-κB signaling pathway.

Parkinson's disease (PD) is associated with both locomotor deficits and gastrointestinal dysfunction, including microbiota dysbiosis and intestinal inflammation. This study investigates the effects of BBr60, a novel strain of high-purity therapeutic Bifidobacterium breve, on intestinal microbiota dysbiosis, intestinal inflammation, and neuroinflammation in PD mice. In animal experiments, we established an in vivo mouse model of Parkinson's disease using 6-hydroxydopamine (6-OHDA) and administered BBr60, along with NLRP3 agonists and inhibitors, via gavage. Behavioral testing was conducted to assess locomotor activity in mice. The 16S rRNA assay was employed to characterize the intestinal microbiota, while gas chromatography-mass spectrometry (GC-MS) was utilized to analyze short-chain fatty acids (SCFA). In cellular experiments, SCFA mixtures formulated according to the SCFA profile observed in animal experiments were administered to RAW264.7 macrophages together with NLRP3 agonists and inhibitors. Western blot (WB) and immunofluorescence (IF) techniques were used for the detection of relevant biomarkers. We found significant microbiota dysbiosis and an imbalance in NLRP3/NLRP6 inflammasomes in the intestine of PD mice. Treatment with BBr60 improved locomotor activity, alleviated microbiota dysbiosis, and increased SCFA in the intestine. BBr60 also restored the NLRP3/NLRP6 balance and inhibited macrophage M1-type polarization in the intestinal environment. Furthermore, SCFAs have been demonstrated to inhibit lipopolysaccharide (LPS)-induced M1-type polarization of macrophages by restoring the balance between NLRP3 and NLRP6 in RAW264.7 macrophages. However, this inhibitory effect was diminished in the presence of an NLRP3 activator. Similarly, the activator of NLRP3 also abrogated the ameliorating effect of BBr60 in intestinal inflammation and neuroinflammation of PD mice. In summary, these findings underscore the pivotal role of the NLRP3/NLRP6 inflammasome and SCFA-mediated signaling in macrophage polarization and intestinal homeostasis. BBr60 may be a promising therapeutic candidate for PD, by ameliorating pathological changes in the intestine.

The gut dysbiosis is associated with the progression of Parkinson's disease (PD). Probiotics have been demonstrated to impact disease progression via the gut-brain axis. This study aims to investigate the therapeutic potential of Akkermansia Muciniphila Akk11 (Akk11) in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. Our results indicated that Akk11 administration significantly improved the MPTP-induced behavioral abnormalities, reduced the loss of dopaminergic neurons, microglia activation, reversed the production of inflammatory cytokines, and colonic damage. Mechanistic studies showed that Akk11 administration suppressed inflammatory responses by inhibiting microglial NLRP3 inflammasome activation. In summary, Akk11 alleviated MPTP-induced motor deficits and neural damage by inhibiting microglial NLRP3 inflammasome. These findings suggest that Akk11 supplementation has therapeutic potential in treating PD through the gut-brain axis.