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Probiotic-directed modulation of gut microbiota is basal microbiome dependent.

ABSTRACT: As an effective means to improve quality of life and prevent diseases, the demand for probiotics and related products has increased in recent years. However, it is still unclear whether a particular probiotic strain will have similar beneficial effects on healthy adults from different regions. In this study, the probiotic Lactobacillus casei Zhang (LCZ) was consumed by healthy adults from six different Asian regions and the changes in gut microbiota were compared using PacBio single molecule, real-time (SMRT) sequencing technology based on samples collected before, during and after consumption of LCZ. Our results reveal that the effect of LCZ consumption on individuals was closely related to the composition of that individual's basal gut microbiota. A Gut Microbiota Variability Index (GMVI) was proposed to quantitatively compare the effects of LCZ on human gut microecology. Subjects from Xinjiang and Singapore regions had the highest and lowest GMVI, respectively. In general, consumption of LCZ increased the relative abundance of certain beneficial bacteria such as Lactobacillus, Roseburia, Coprococcus and Eubacterium rectale, while it inhibited growth of certain harmful bacteria such as Blautia and Ralstonia pickettii. In addition, consumption of LCZ was responsible for the conversion of some participants from Prevotella copri/Faecalibacterium prausnitzii (PF) enterotype to Faecalibacterium prausnitzii/Bacteroides dorei (FB) enterotype and consistently increased the abundance of lactic acid bacteria in the gut. It also increased/enhanced phosphate metabolic modules, amino acid transport systems, and isoleucine biosynthesis, but conversely decreased lipopolysaccharide biosynthesis. These changes could have health benefits for healthy adults.

SUBMITTER: Hou Q

PROVIDER: S-EPMC7524168 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:The influence of dietary factors on brain health and mental function is becoming increasingly recognized. Similarly, mounting evidence supports a role for gut microbiota in modulating central nervous system function and behaviour. Still, the molecular mechanisms responsible for the impact of diet and associated microbiome in adult neurodegeneration are still largely unclear. In this study, we aimed to investigate whether and how changes in diet-associated microbiome and its metabolites impact on adult neurogenesis. Mice were fed a high-fat, choline-deficient diet, developing obesity and several features of the metabolic syndrome, including non-alcoholic steatohepatitis. Strikingly, our results showed, for the first time, that animals fed with this specific diet display premature increased neurogenesis, possibly exhausting the available neural stem cell pool for long-term neurogenesis processes. The high-fat, choline-deficient diet further induced neuroinflammation, oxidative stress, synaptic loss and cell death in different regions of the brain. Notably, this diet-favoured gut dysbiosis in the small intestine and cecum, up-regulating metabolic pathways of short-chain fatty acids, such as propionate and butyrate and significantly increasing propionate levels in the liver. By dissecting the effect of these two specific short-chain fatty acids in vitro, we were able to show that propionate and butyrate enhance mitochondrial biogenesis and promote early neurogenic differentiation of neural stem cells through reactive oxygen species- and extracellular signal-regulated kinases 1/2-dependent mechanism. More importantly, neurogenic niches of high-fat, choline-deficient-fed mice showed increased expression of mitochondrial biogenesis markers, and decreased mitochondrial reactive oxygen species scavengers, corroborating the involvement of this mitochondrial stress-dependent pathway in mediating changes of adult neurogenesis by diet. Altogether, our results highlight a mitochondria-dependent pathway as a novel mediator of the gut microbiota-brain axis upon dietary influences.

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Probiotic-directed modulation of gut microbiota is basal microbiome dependent.

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