Gut bacteria
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ABSTRACT:
PROVIDER: PRJNA1093465 | ENA |
REPOSITORIES: ENA
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Project description:Symbiotic bacteria inhabiting the distal human gut have evolved under intense pressure to utilize complex carbohydrates, predominantly plant cell wall glycans abundant in our diets. These substrates are recalcitrant to depolymerization by digestive enzymes encoded in the human genome, but are efficiently targeted by some of the ~103-104 bacterial species that inhabit this niche. These species augment our comparatively narrow carbohydrate digestive capacity by unlocking otherwise unusable sugars and fermenting them into host-absorbable forms, such as short-chain fatty acids. We used phenotype profiling, whole-genome transcriptional analysis and molecular genetic approaches to investigate complex glycan utilization by two fully sequenced and closely related human gut symbionts: Bacteroides thetaiotaomicron and Bacteroides ovatus. Together these species target all of the common glycosidic linkages found in the plant cell wall, as well as host polysaccharides, but each species exhibits a unique ‘glycan niche’: in vitro B. thetaiotaomicron targets plant cell wall pectins in addition to linkages contained in host N- and O-glycans; B. ovatus uniquely targets hemicellulosic polysaccharides along with several pectins, but is deficient in host glycan utilization. Bacteroides ovatus bacteria were grown either in vitro on defined complex glycan sources, or in vivo in the intestinal tract of gnotobiotic mice fed variable diets. Increased in vitro gene expression was used to indicate the genes required for metabolism of complex glycans and compared to in vivo transcriptional activity to determine expression in the mouse gut.
2011-05-01 | E-GEOD-25575 | biostudies-arrayexpress
Project description:Symbiotic bacteria inhabiting the distal human gut have evolved under intense pressure to utilize complex carbohydrates, predominantly plant cell wall glycans abundant in our diets. These substrates are recalcitrant to depolymerization by digestive enzymes encoded in the human genome, but are efficiently targeted by some of the ~103-104 bacterial species that inhabit this niche. These species augment our comparatively narrow carbohydrate digestive capacity by unlocking otherwise unusable sugars and fermenting them into host-absorbable forms, such as short-chain fatty acids. We used phenotype profiling, whole-genome transcriptional analysis and molecular genetic approaches to investigate complex glycan utilization by two fully sequenced and closely related human gut symbionts: Bacteroides thetaiotaomicron and Bacteroides ovatus. Together these species target all of the common glycosidic linkages found in the plant cell wall, as well as host polysaccharides, but each species exhibits a unique ‘glycan niche’: in vitro B. thetaiotaomicron targets plant cell wall pectins in addition to linkages contained in host N- and O-glycans; B. ovatus uniquely targets hemicellulosic polysaccharides along with several pectins, but is deficient in host glycan utilization.
2011-05-01 | GSE25575 | GEO
Project description:Symbiotic bacteria inhabiting the distal human gut have evolved under intense pressure to utilize complex carbohydrates, predominantly plant cell wall glycans abundant in our diets. These substrates are recalcitrant to depolymerization by digestive enzymes encoded in the human genome, but are efficiently targeted by some of the ~103-104 bacterial species that inhabit this niche. These species augment our comparatively narrow carbohydrate digestive capacity by unlocking otherwise unusable sugars and fermenting them into host-absorbable forms, such as short-chain fatty acids. We used phenotype profiling, whole-genome transcriptional analysis and molecular genetic approaches to investigate complex glycan utilization by two fully sequenced and closely related human gut symbionts: Bacteroides thetaiotaomicron and Bacteroides ovatus. Together these species target all of the common glycosidic linkages found in the plant cell wall, as well as host polysaccharides, but each species exhibits a unique ‘glycan niche’: in vitro B. thetaiotaomicron targets plant cell wall pectins in addition to linkages contained in host N- and O-glycans; B. ovatus uniquely targets hemicellulosic polysaccharides along with several pectins, but is deficient in host glycan utilization.
2011-05-01 | GSE25572 | GEO
Project description:The adult human gut microbial community is typically dominated by two bacterial phyla (divisions), the Firmicutes and the Bacteroidetes. Little is known about the factors that govern the interactions between their members. Here we examine the niches of representatives of both phyla in vivo. Finished genome sequences were generated from E. rectale and E. eligens, which belong to Clostridium Cluster XIVa, one of the most common gut Firmicute clades. Comparison of these and 25 other gut Firmicutes and Bacteroidetes indicated that the former possess smaller genomes and a disproportionately smaller number of glycan-degrading enzymes. Germ-free mice were then colonized with E. rectale and/or a prominent human gut Bacteroidetes, Bacteroides thetaiotaomicron, followed by whole genome transcriptional profiling of both organisms in their distal gut (cecal) habitat as well as host responses, high resolution proteomic analysis of cecal contents, and biochemical assays of carbohydrate metabolism. B. thetaiotaomicron adapts to E. rectale by upregulating expression of a variety of polysaccharide utilization loci (PULs) encoding numerous glycoside hydrolase gene families, and by signaling the host to produce mucosal glycans that it, but not E. rectale, can access. E. rectale adapts to B. thetaiotaomicron by decreasing production of its glycan-degrading enzymes, increasing expression of selected amino acid and sugar transporters, and facilitating glycolysis by reducing levels of NADH, in part via generation of butyrate from acetate, which in turn is utilized by the gut epithelium. This simplified model of the human gut microbiota illustrates niche specialization and functional redundancy within members of major gut bacterial phyla, and the importance of host glycans as a nutrient foundation that ensures ecosystem stability. The interactions between E. rectale and B. thetaiotaomicron were characterized by performing whole genome transcriptional profiling of each species after colonization of gnotobiotic mice with each organism alone, or in combination. E. rectale was also profiled during in vitro growth.
2010-05-22 | E-GEOD-14737 | biostudies-arrayexpress
Project description:Symbiotic bacteria inhabiting the distal human gut have evolved under intense pressure to utilize complex carbohydrates, predominantly plant cell wall glycans abundant in our diets. These substrates are recalcitrant to depolymerization by digestive enzymes encoded in the human genome, but are efficiently targeted by some of the ~103-104 bacterial species that inhabit this niche. These species augment our comparatively narrow carbohydrate digestive capacity by unlocking otherwise unusable sugars and fermenting them into host-absorbable forms, such as short-chain fatty acids. We used phenotype profiling, whole-genome transcriptional analysis and molecular genetic approaches to investigate complex glycan utilization by two fully sequenced and closely related human gut symbionts: Bacteroides thetaiotaomicron and Bacteroides ovatus. Together these species target all of the common glycosidic linkages found in the plant cell wall, as well as host polysaccharides, but each species exhibits a unique ‘glycan niche’: in vitro B. thetaiotaomicron targets plant cell wall pectins in addition to linkages contained in host N- and O-glycans; B. ovatus uniquely targets hemicellulosic polysaccharides along with several pectins, but is deficient in host glycan utilization. Growth of Bacteroides thetaiotaomicron in vitro in minimal medium plus different purified complex glycans. Observation of increased gene expression was used to determine genes that are involved in metabolism of each glycan. Two biological replicates each.
2011-05-01 | E-GEOD-25572 | biostudies-arrayexpress
Project description:Aim: Microbial colonization of the intestine in newborns is a critical event that regulates host physiology with lifelong consequences. However, there is a need to identify microbial molecules and mechanisms that play a role in this process. We aimed to elucidate the effects of flagellin, an important immunomodulatory component involved in bacterial motility, on intestinal epithelial functions. Methods: Germfree mice were colonized with synthetic bacterial communities, including a flagellated mouse gut isolate of Escherichia coli or a ΔfliC mutant thereof that lacks flagella. The offspring of these mice were studied at 7 days of age by single-cell RNA sequencing of epithelial cells isolated from the small intestine. Results: Enterococcus faecalis was the most dominant species in the small intestine of newborn mice. Blautia pseudococcoides was detected at low relative abundances. Colonization by either E. coli strain reduced the relative abundance of E. faecalis to 10% on average, and E. coli became the dominant member, with no substantial differences between mice colonized with the wildtype or mutant strain. The distribution of cell types within the small intestinal epithelium was skewed toward specialized cells (goblet, enteroendocrine, stem cells) at the expense of enterocytes in mice colonized with flagellated bacteria. These mice were characterized by higher expression of genes involved in cell-cell interactions (Npl, Epcam) and responses to infection (Ctsl) in enterocytes and enhanced translation (ribosomal proteins) in stem cells. In contrast, genes involved in lipid homeostasis (transport and metabolism; Apoc 2/4, Dgat2, Fabp 1/2, Mttp) in all cell types and inflammatory and androgen-related pathways in specialized cell types were less expressed in epithelial cells exposed to wildtype E. coli. Conclusion: These findings suggest that early life exposure to flagellated commensal bacteria influences cellular processes underlying tissue metabolism and remodeling in the small intestine.
2024-04-21 | GSE264411 | GEO
Project description:The host genotype has been proposed to contribute to individually composed bacterial communities in the gut. To provide deeper insight into interactions between gut bacteria and their host, we associated germ-free C3H and C57BL/10 mice with intestinal bacteria from a C57BL/10 donor mouse. Analysis of microbiota similarity between the experimental animals with denaturing gradient gel electrophoresis (DGGE) 13 weeks after association revealed the development of a mouse strain specific microbiota. Gene expression in the colonic mucosa was analyzed with a microarray approach taking advantage of a modified Affymetrix mouse genome chip. We detected 202 genes whose expression differed significantly by a factor of < 2. Application of bioinformatics tools demonstrated that functional terms including signaling/secretion, lipid degradation/catabolism, guanine nucleotide/guanylate binding and immune response were significantly enriched in differentially expressed genes. We had a closer look at the 56 genes with expression differences of < 4 and observed a higher expression in C57BL/10 mice of the genes coding for toll-like receptor 1 (4-fold) and angiogenin 4 (33-fold) which are involved in the recognition and response to gut bacteria. In contrast, a 70-fold higher expression of the phospholipase A2, group IIA-encoding gene (Pla2g2a) was detected in C3H mice. In addition, a number of interferon-inducible genes were higher expressed in C3H than in C57BL/10 mice including Gbp1 (18-fold), Mal (7-fold), Oasl2 (7-fold), Ifi202b (7-fold), Rtp4 (6-fold), Ly6g6c (5-fold), Ifi27l2a (5-fold), Usp18 (5-fold), Ifit1 (5-fold), Ifi44 (4-fold), and Ly6g (4-fold) indicating that these cytokines play an essential role in microbiota regulation. However, genes coding for interferons, their receptors or factors involved in interferon signaling pathways were not differentially expressed between the two mouse strains. Taken together, our study confirms that the host genotype is involved in the establishment of host-specific bacterial communities in the gut. Based on expression differences after colonization with the same bacterial inoculum, we propose that Pla2g2a and interferon-dependent genes may contribute to this phenomenon. Total RNA was extracted from the colonic mucosa and hybridization was performed using 12.5M-BM- M-bM-^@M-^SM-BM- 20M-BM- M-BM-5g of cDNA on a customized Affymetrix nugomm 1a520177 chip.
2013-04-09 | E-GEOD-45876 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE25572: Depolymerization of plant cell wall glycans by symbiotic human gut bacteria (Bacteroides thetaiotaomicron) GSE25575: Depolymerization of plant cell wall glycans by symbiotic human gut bacteria (Bacteroides ovatus) Refer to individual Series
2011-05-01 | E-GEOD-25576 | biostudies-arrayexpress
Project description:The adult human gut microbial community is typically dominated by two bacterial phyla (divisions), the Firmicutes and the Bacteroidetes. Little is known about the factors that govern the interactions between their members. Here we examine the niches of representatives of both phyla in vivo. Finished genome sequences were generated from E. rectale and E. eligens, which belong to Clostridium Cluster XIVa, one of the most common gut Firmicute clades. Comparison of these and 25 other gut Firmicutes and Bacteroidetes indicated that the former possess smaller genomes and a disproportionately smaller number of glycan-degrading enzymes. Germ-free mice were then colonized with E. rectale and/or a prominent human gut Bacteroidetes, Bacteroides thetaiotaomicron, followed by whole genome transcriptional profiling of both organisms in their distal gut (cecal) habitat as well as host responses, high resolution proteomic analysis of cecal contents, and biochemical assays of carbohydrate metabolism. B. thetaiotaomicron adapts to E. rectale by upregulating expression of a variety of polysaccharide utilization loci (PULs) encoding numerous glycoside hydrolase gene families, and by signaling the host to produce mucosal glycans that it, but not E. rectale, can access. E. rectale adapts to B. thetaiotaomicron by decreasing production of its glycan-degrading enzymes, increasing expression of selected amino acid and sugar transporters, and facilitating glycolysis by reducing levels of NADH, in part via generation of butyrate from acetate, which in turn is utilized by the gut epithelium. This simplified model of the human gut microbiota illustrates niche specialization and functional redundancy within members of major gut bacterial phyla, and the importance of host glycans as a nutrient foundation that ensures ecosystem stability.
2009-03-01 | GSE14737 | GEO
Project description:Morphine and its pharmacological derivatives are the most prescribed analgesics for moderate to severe pain management. However, chronic use of morphine reduces pathogen clearance and induces bacterial translocation across the gut barrier. The enteric microbiome has been shown to play a critical role in the preservation of the mucosal barrier function and metabolic homeostasis. Here, we show for the first time, using bacterial 16s rDNA sequencing, that chronic morphine treatment significantly alters the gut microbial composition and induces preferential expansion of the gram-positive pathogenic and reduction of bile-deconjugating bacterial strains. A significant reduction in both primary and secondary bile acid levels was seen in the gut, but not in the liver with morphine treatment. Morphine induced microbial dysbiosis and gut barrier disruption was rescued by transplanting placebo-treated microbiota into morphine-treated animals, indicating that microbiome modulation could be exploited as a therapeutic strategy for patients using morphine for pain management. In this study, we establish a link between the two phenomena, namely gut barrier compromise and dysregulated bile acid metabolism. We show for the first time that morphine fosters significant gut microbial dysbiosis and disrupts cholesterol/bile acid metabolism. Changes in the gut microbial composition is strongly correlated to disruption in host inflammatory homeostasis13,14 and in many diseases (e.g. cancer/HIV infection), persistent inflammation is known to aid and promote the progression of the primary morbidity. We show here that chronic morphine, gut microbial dysbiosis, disruption of cholesterol/bile acid metabolism and gut inflammation; have a linear correlation. This opens up the prospect of devising minimally invasive adjunct treatment strategies involving microbiome and bile acid modulation and thus bringing down morphine-mediated inflammation in the host.
2016-06-01 | E-MTAB-3722 | biostudies-arrayexpress