Project description:Bifidobacteria is strongly associated with human health and dominates the gut microbiota of breast-fed infants. However, Bifidobacteria persists at high abundance in only a subset of individuals after weaning, and the factors that regulate intestinal persistence of Bifidobacteria are poorly understood. Here, we identified that a common dietary fiber, raffinose, supports Bifidobacteria persistence within complex microbiome communities. Raffinose-driven Bifidobacteria persistence is associated with disease resistance and restrained inflammation in mice. Altogether, our findings show that raffinose selectively regulates the intestinal persistence of Bifidobacteria, which may enable its sustained maintenance during microbiome diversification and thereby support prolonged probiotic functions.
Project description:Bifidobacteria is strongly associated with human health and dominates the gut microbiota of breast-fed infants. However, Bifidobacteria persists at high abundance in only a subset of individuals after weaning, and the factors that regulate intestinal persistence of Bifidobacteria are poorly understood. Here, we identified that a common dietary fiber, raffinose, supports Bifidobacteria persistence within complex microbiome communities. Raffinose-driven Bifidobacteria persistence is associated with disease resistance and restrained inflammation in mice. Altogether, our findings show that raffinose selectively regulates the intestinal persistence of Bifidobacteria, which may enable its sustained maintenance during microbiome diversification and thereby support prolonged probiotic functions.
Project description:Bifidobacteria is strongly associated with human health and dominates the gut microbiota of breast-fed infants. However, Bifidobacteria persists at high abundance in only a subset of individuals after weaning, and the factors that regulate intestinal persistence of Bifidobacteria are poorly understood. Here, we identified that a common dietary fiber, raffinose, supports Bifidobacteria persistence within complex microbiome communities. Raffinose-driven Bifidobacteria persistence is associated with disease resistance and restrained inflammation in mice. Altogether, our findings show that raffinose selectively regulates the intestinal persistence of Bifidobacteria, which may enable its sustained maintenance during microbiome diversification and thereby support prolonged probiotic functions.
Project description:We report that cellular ROS enzymatically generated in response to contact with lactobacilli in both mice and Drosophila has salutary effects against exogenous insults to the intestinal epithelium via the activation of Nrf2 responsive cytoprotective genes.
Project description:We report that cellular ROS enzymatically generated in response to contact with lactobacilli in both mice and Drosophila has salutary effects against exogenous insults to the intestinal epithelium via the activation of Nrf2 responsive cytoprotective genes.
Project description:Development of the human gut microbiota commences at birth, with bifidobacteria being among the first colonizers of the newborn gastrointestinal tract. To date, the genetic basis of Bifidobacterium colonization, persistence and dialogue with the host remains poorly understood. We previously identified tight adherence (Tad) pili from Bifidobacterium breve UCC2003 as an essential colonisation factor using murine models.We have identified the protein that mediates the proliferation response, and demonstrate that bifidobacteria contribute to the maturation of the naïve gut in early life through the production of specific extracellular protein structures under in vivo conditions. This bifidobacteria-derived signalling protein may represent one of the mechanisms by which members of the early colonising microbiota stimulate growth of the neonatal mucosa
Project description:We report that cellular ROS enzymatically generated in response to contact with lactobacilli in both mice and Drosophila has salutary effects against exogenous insults to the intestinal epithelium via the activation of Nrf2 responsive cytoprotective genes. RNA was isolated from the colons of untreated, PBS, E. coli, and LGG innoculated germ free mice and RNA-seq performed to identify the gene expression in response to each condition