Microbial niches in raw ingredients determine microbial community assembly during kimchi fermentation.

Fermented foods constitute hubs of microbial consortia differentially affecting nutritional and organoleptic properties, quality, and safety. Here we show the origin source of fermentative microbes and fermentation dynamics of kimchi. We partitioned microbiota by raw ingredient (kimchi cabbage, garlic, ginger, and red pepper) to render kimchi fermented by each source-originated microbe pool and applied multi-omics (metataxonomics and metabolomics), bacterial viability, and physiochemical analyses to longitudinally collected samples. Only kimchi cabbage- and garlic-derived microbial inoculums yielded successful kimchi fermentations. The dominant fermentative microbial taxa and subsequent metabolic outputs differed by raw ingredient type: the genus Leuconostoc, Weissella, and Lactobacillus for all non-sterilized ingredients, garlic, and kimchi cabbage, respectively. Gnotobiotic kimchi inoculated by mono-, di-, and tri- isolated fermentative microbe combinations further revealed W. koreensis-mediated reversible microbial metabolic outputs. The results suggest that the raw ingredient microbial habitat niches selectively affect microbial community assembly patterns and processes during kimchi fermentation.

Oral Administration of Gintonin Attenuates Cholinergic Impairments by Scopolamine, Amyloid-ß Protein, and Mouse Model of Alzheimer's Disease.

Gintonin is a novel ginseng-derived lysophosphatidic acid (LPA) receptor ligand. Oral administration of gintonin ameliorates learning and memory dysfunctions in Alzheimer's disease (AD) animal models. The brain cholinergic system plays a key role in cognitive functions. The brains of AD patients show a reduction in acetylcholine concentration caused by cholinergic system impairments. However, little is known about the role of LPA in the cholinergic system. In this study, we used gintonin to investigate the effect of LPA receptor activation on the cholinergic system in vitro and in vivo using wild-type and AD animal models. Gintonin induced [Ca(2+)]i transient in cultured mouse hippocampal neural progenitor cells (NPCs). Gintonin-mediated [Ca(2+)]i transients were linked to stimulation of acetylcholine release through LPA receptor activation. Oral administration of gintonin-enriched fraction (25, 50, or 100 mg/kg, 3 weeks) significantly attenuated scopolamine-induced memory impairment. Oral administration of gintonin (25 or 50 mg/kg, 2 weeks) also significantly attenuated amyloid-ß protein (Aß)-induced cholinergic dysfunctions, such as decreased acetylcholine concentration, decreased choline acetyltransferase (ChAT) activity and immunoreactivity, and increased acetylcholine esterase (AChE) activity. In a transgenic AD mouse model, long-term oral administration of gintonin (25 or 50 mg/kg, 3 months) also attenuated AD-related cholinergic impairments. In this study, we showed that activation of G protein-coupled LPA receptors by gintonin is coupled to the regulation of cholinergic functions. Furthermore, this study showed that gintonin could be a novel agent for the restoration of cholinergic system damages due to Aß and could be utilized for AD prevention or therapy.