Wecare Probiotics Co., Ltd.

This research delved into the feasibility of utilizing three nanochitin-chitin nanocrystal (CNC), chitin nanofiber (CNF), and chitin nanosphere (CNS) in complexation with whey protein isolate (WPI) to fabricate complex coacervation and create microcapsules for probiotic encapsulation. The results showed that CNC, CNF, and CNS exhibited notable differences in morphologies, dimensions, and properties due to the respective synthesis methodologies. Nevertheless, all of them maintained a positive charge and were capable of assembling into microcapsules with WPI via electrostatic interactions at optimal pHs. The inclusion of Lactobacillus casei (L. casei) during the complex coacervation phase engendered a shell-like formation around the bacterium within the microcapsule, which enhanced probiotic viability and increased colony-forming unit count. Additionally, these probiotic-loading microcapsules were also processed into tablets, displaying robust structural integrity, augmented protective capabilities, and a distinctive sustained-release profile compared to the microcapsules alone. In summary, this study pioneered the employment of nanochitin formulations in complex coacervation to encapsulate L. casei, spearheading an innovative approach to the creation of a compressed probiotic supplement and contributing to the advancement in the design and fabrication of encapsulation vehicles for active ingredients.

Bifidobacterium animalis subsp. lactis BLa80 is a new probiotic strain with extensive applications in food products both domestically and internationally. Given the rising consumption of this probiotic, its safety assessment is increasingly crucial in the food industry. This study evaluates the safety of strain BLa80 using a combination of in vitro and in vivo assays along with genomic analysis. Methods included exposing the strain to artificial gastric and intestinal fluids, as well as a medium containing bile salts, to stimulate human digestive conditions. The strain showed high tolerance to gastric fluid at pH of 2.5 and to 0.3 % bile salts. It maintained a 99.92 % survival rate in intestinal fluid. Additional tests assessed hemolytic activity, antibiotic susceptibility (revealing sensitivity to 7 antibiotics), and biogenic amine production using HPLC-ELSD, confirming the absence of histamine, and other harmful amines. Bile salt hydrolase activity was demonstrated qualitatively, and metabolic byproducts were quantitatively analyzed using a D-/l-lactic acid assay kit, showing that BLa80 produces 1.48 mg/mL of l-lactic acid and no harmful d-lactic acid. Genomic analysis confirmed the absence of virulence or pathogenicity genes, and a 90-day oral toxicity study in rats confirmed no toxic effects at various doses. Overall, these findings support the safety classification of the strain BLa80.

This study investigated the effect of Lacticaseibacillus rhamnosus LRa05 on alcoholic fatty liver disease (ALD) and its mechanism for liver protection. Mice were randomly divided into three groups: a control (CLT) group, an ALD group, and a LRa05 intervention group. The ALD mouse model was established by Lieber-DeCarli chronic alcohol feeding. Tissues staining, enzyme-linked immunosorbent assay (ELISA) was performed to detect changes in histopathology and inflammatory cytokines, respectively. Moreover, intestinal permeability was evaluated by the level of dextran-fluorescein isothiocyanate (Dx-FITC) in serum and tight junction protein in the colon. Changes in the composition of the gut microbiota were assessed by 16S rRNA sequencing. Alcohol consumption induced liver damage in mice with significantly increased levels of triglycerides (TG), aspartate aminotransferase (AST), alanine transaminase (ALT), and inflammatory cytokines. Moreover, alcohol further induced the increase of intestinal permeability and disruption of gut microbiota in mice, with an increase in the relative abundance of potentially pathogenic bacteria Enterococcus, Parabacteroides, and Alistipes. LRa05 intervention significantly attenuated alcohol-induced liver injury by reducing the contents of TG, ALT, and AST, and suppressing the inflammatory responses. Meanwhile, by stimulating the expression of ZO-1, Occludin, and Claudin in the colon tissue, LRa05 additionally strengthened the intestine barrier function. Furthermore, gut microbiota analysis suggested that LRa05 partially ameliorated gut microbiota disorders in ALD mice and up-regulated the abundance of Desulfovibrio and Akkermansia, which were negatively correlated with the indicators of ALD progression. The reconstructive effects of LRa05 on the gut microbiota might be related to the efficacy of LRa05 in improving gut permeability and further protecting against ALD.