Ulcerative colitis (UC) is primarily associated with disruptions in the intestinal barrier function and dysbiosis of the gut microbiota. Utilizing probiotics to modulate intestinal barrier integrity and restore gut microbiota balance has emerged as a promising approach for both preventing and treating UC. Nonetheless, the harsh gastrointestinal (GI) environment and rapid passage of body fluids often reduce the viability and colonization of unencapsulated probiotics in the gut. Drawing inspiration from the protective properties of biofilms, we utilized a self- produced biofilm to act as a protective "armor" for the probiotic strain Bacillus paralicheniformis, enhancing its tolerance to the GI tract and its ability to colonize sites of inflammatory bowel disease. In our approach, the biofilm-coated B. paralicheniformis (BCBP) demonstrated significant therapeutic efficacy in UC mice. Compared to uncoated B. paralicheniformis (BP), BCBP exhibited a 4.3-fold increase in survival rate following a 2-hour exposure to simulated gastric fluid. Moreover, BCBP colonization at sites of intestinal inflammation was 2.7-fold higher than that of BP. Importantly, the extracellular polymeric substances within the biofilm bolstered the strain's ability to fortify the intestinal barrier, mitigate inflammation, and restore gut microbiota balance, thereby exerting a synergistic effect in alleviating UC symptoms. In summary, this study not only offers a bio-inspired delivery strategy with strong potential for the treatment of UC, but also proposes a novel paradigm for the delivery of probiotics in the form of biofilms.

Pomegranate seed oil (PSO) mainly consisted of punicic acid (PunA), has gained attention due to rich conjugated linolenic acids and potential application in the improvement of various diseases. The aim of this study was to explore the ability of PunA to modulate lipid metabolism associated with non-alcoholic fatty liver disease (NAFLD) and explore the emerging role of the gut microbiota in modulating hepatic lipid metabolism. In this regard, PunA's capacity was evaluated through C57BL/6J fed with a choline and L-amino acid defined high fat diet (CDAHFD). Mice were randomly divided into 4 groups and fed with control diet (low fat diet), CDAHFD + 2% PSO, CDAHFD + 0.2% curcumin (Cur) + 2% corn oil (positive control), or vehicle alone (CDAHFD + 2% corn oil). Collected results indicated that supplement of PunA improved hepatic lipid profile. PunA administration also ameliorated hepatic steatosis and lipid accumulation. mRNA analysis showed that PunA exerted ameliorative effect on hepatic lipid accumulation by downregulating the mRNA expression of Dgat1, Scd-1, Srebp-1c, but increasing expression level of Cpt-1α. Metagenomic analysis discovered that PunA increased species diversity and richness of intestinal microbiota, promoted proliferation of beneficial commensals and restraining the endotoxin-producing microorganisms in cecum of CDAHFD-administrated mice. Furthermore, PunA suppressed lipid accumulation and lipid droplet formation in a cell NAFLD model in vitro. Overall, PunA exhibited anti-lipogenic and lipid-lowering effects, improvement of intestinal flora. In summary, PunA could be a candidate for the exploitation of functional foods or nutraceuticals aiming NAFLD.

An unknown laboratory strain was identified and named as Bacillus cereus HMPM18123 based on the 16S rRNA gene and conserved protein-coding gene (gyrA and gyrB) sequences combined with virulence genes (nheA, nheB, nheC, hblA, hblC, hblD, becT, cytK and entFM) and biochemical properties. The tolerance of the strain to different temperatures, pH, simulated gastric and intestinal fluid was evaluated as well as its efficacy in alleviating colitis induced by dextran sulfate sodium (DSS) in mice. The results of growth characteristics showed that the strain had good tolerance to high temperature and simulated gastric and intestinal fluid. In addition, the strain improved DSS-induced colitis symptoms in mice such as body mass loss, colon shortening, increased disease activity index (DAI) score, tissue lesions, and up-regulated expression of inflammatory factors.