Project description:Pu-erh tea has attracted increasing attention worldwide because of its special flavor and health effects, but its impact on composition and function of the gut microbiota remains unclear. The aim of this study was to investigate effects of aqueous extracts of fermented (ripe) and non-fermented (raw) Pu-erh teas on the composition and function of intestinal microbiota of rats with diet-induced obesity. We conducted a comparative metagenomic and metaproteomic investigation of the microbial communities in cecal samples taken from obese rats administrated with or without extracts of raw and ripe Pu-erh tea. By analyzing the composition and diversity of 16S rRNA amplicons and expression profiles of 814 distinct proteins, we found that, despite differences in the chemical compositions of the raw and ripe Pu-erh tea, administration of either at two different doses (0.15 and 0.40 g/Kg body weight), significantly (P<0.05) increased community diversity, and changed the composition of the cecal microbiota by increasing the relative abundances of Firmicutes and decreasing those of Bacteroidetes. Community metabolic processes including sucrose metabolism, glycolysis, syntheses of proteins, rRNA and antibiotics were significantly (P<0.05), or had a tendency (0.10<P<0.05) to be, promoted by enriching relevant enzymes. Furthermore, evidences from population, molecular and metabolic levels have shown that polyphenols of raw Pu-erh tea and their metabolites can promote potentially the growth of Akkermansia municiphila by stimulating the type II and III secretion system protein, elongation factor Tu, and glyceraldehyde-3-phosphate dehydrogenase. This study has provided new evidences for the prebiotic effects of Pu-erh tea.
Project description:Neonatal mice were susceptible to cryptosporidium infection at 1- and 2-weeks of age, but were resistant to infection at 3- and 6-weeks of age. Diet and microbial changes are known to occur during the weaning transition in mice and we hypothesized that these changes in the intestinal luminal environment might influence resistance and susceptibility to cryptosporidium infection. As one part of testing this hypothesis, cecal microbiota composition was determined by 16S ribosomal RNA sequencing of DNA isolated from the cecal contents of mice at 1 week, 2 weeks, 3 weeks, and 6 weeks of age.
Project description:The interplay between the intestinal microbiota and host is critical to intestinal ontogeny and homeostasis. MicroRNAs (miRNAs) may be an underlying link. Intestinal miRNAs are microbiota-dependent and when shed in the lumen, affect resident microorganisms. Yet, longitudinal relationships between intestinal tissue miRNAs, luminal miRNAs, and luminal microorganisms have not been elucidated, especially in early life. Here, we investigated the postnatal cecal miRNA and microbiota populations, their relationship, and their impact on intestinal maturation in specific and opportunistic pathogen free mice; we also assessed if they can be modified by an intervention with allochthonous probiotic lactobacilli. We report that cecal and cecal content miRNA and microbiota signatures are temporally regulated, correlated, and modifiable by probiotics with implications for intestinal maturation. These findings help with understanding causal relationships within the gut ecosystem and provide a basis for preventing and managing their alterations in diseases throughout life.
Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model. Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration. The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors. CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing. Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota. This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury.
Project description:Microbial RNAseq analysis of cecal and fecal samples collected from mice colonized with the microbiota of human twins discordant for obesity. Samples were colleted at the time of sacrifice, or 15 days after colonization from mice gavaged with uncultured or cultured fecal microbiota from the lean twins or their obese co-twins. Samples were sequenced using Illumina HiSeq technology, with 101 paired end chemistry. Comparisson of microbial gene expression between the microbiota of lean and obese twins fed a Low fat, rich in plant polysaccharide diet.
Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury
Project description:Early-life antibiotic exposure perturbs the intestinal microbiota, alters innate intestinal immunity, and accelerates type 1 diabetes development in the NOD mouse model. Here we found that maternal cecal microbiota transfer (CMT) to NOD mice with early-life antibiotic perturbation partially rescued the induced T1D acceleration. The restoration effects on the intestinal microbiome were substantial and persistent, remediating the antibiotic-depleted diversity, relative abundance of particular taxa, and metabolic pathways. CMT also protected against perturbed cecal and serum metabolites and normalized innate and adaptive immune effectors. CMT restored patterns of ileal microRNA and histone regulation of gene expression and exon-splicing. Based on the analyses of experimental data, we propose an innate intestinal immune network involving CD44, TLR2, and Reg3g, as well as their multiple microRNA and epigenetic regulators that sense intestinal signaling by the gut microbiota. This regulation affects downstream immunological tone, leading to protection against the tissue-specific T1D injury.