Highly active probiotic hydrogels matrixed on bacterial EPS accelerate wound healing via maintaining stable skin microbiota and reducing inflammation.

Skin microbiota plays an important role in wound healing, but skin injuries are highly susceptible to wound infections, leading to disruption of the skin microbiota. However, conventional antibacterial hydrogels eliminate both probiotics and pathogenic bacteria, disrupting the balance of the skin microbiota. Therefore, it is important to develop a wound dressing that can fend off foreign pathogenic bacteria while preserving skin microbiota stability. Inspired by live bacteria therapy, we designed a probiotic hydrogel (HAEPS@L.sei gel) with high viability for promoting wound healing. Lactobacillus paracasei TYM202 encapsulated in the hydrogel has the activity of promoting wound healing, and the hydrogel matrix EPS-M76 has the prebiotic activity that promotes the proliferation and metabolism of Lactobacillus paracasei TYM202. During the wound healing process, HAEPS@L.sei gel releases lactic acid and acetic acid to resist the growth of pathogenic bacteria while maintaining Firmicutes and Proteobacteria balance at the phylum level, thus preserving skin microbiota stability. Our results showed that live probiotic hydrogels reduce the incidence of inflammation during wound healing while promoting angiogenesis and increasing collagen deposition. This study provides new ideas for developing wound dressings predicated on live bacterial hydrogels.

Fucogalactan Sulfate (FS) from Laminaria japonica Regulates Lipid Metabolism in Diet-Induced Humanized Dyslipidemia Mice via an Intestinal FXR-FGF19-CYP7A1/CYP8B1 Pathway.

Our previous study found that fucogalactan sulfate (FS) from Laminaria japonica exhibited significant hypolipidemic effects. To further elucidate the mechanism, we first constructed a dyslipidemia mouse model with humanized gut microbiota and proved the main differential metabolic pathway involved bile acid metabolism. Then, we evaluated the beneficial effects of FS on dyslipidemia in this model mice, which revealed that oral FS administration reduced serum cholesterol levels and mitigated liver fat accumulation. Gut microbiota and microbiome analysis showed FS increased the abundance of Ruminococcaceae_NK4A214_group, GCA-900066755, and Eubacterium, which were positively associated with the fecal DCA, ß-MCA, and HDCA. Further investigation demonstrated that FS inhibited the hepatic farnesoid X receptor (FXR), while activating the intestinal FXR-FGF19 pathway, leading to suppression of CYP7A1 and CYP8B1, as well as potentially reduced bile acid synthesis and lipid absorption. Overall, FS regulated lipid metabolism in diet-induced humanized dyslipidemia mice via the bile acid-mediated intestinal FXR-FGF19-CYP7A1/CYP8B1 pathway.