Bacteria
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ABSTRACT:
PROVIDER: PRJNA482748 | ENA |
REPOSITORIES: ENA
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Project description:Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Using gnotobiotic mouse models, we provide a systematic analysis of the role of microbiota in the induction of cytokine responses in the normal intestine. Colonization by a whole mouse microbiota orchestrated a broad spectrum of pro-inflammatory (Th1, Th17) and regulatory T cell responses. Unexpectedly, most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal cytokine responses. A potent cytokine-inducing function was however associated with non-culturable host-specific species, the prototype of which was the Clostridia-related Segmented Filamentous Bacterium, and this bacterial species recapitulated the coordinated maturation of T cell responses induced by the whole mouse microbiota. Our study demonstrates the non-redundant role of microbiota members in the regulation of gut immune homeostasis. Germfree (GF) female 8-9-week-old mice were gavaged twice at a 24-hr interval with 0.5 mL of fresh anaerobic cultures of fecal homogenate from SFB mono-associated mice, fresh feces from Cv mice (Cvd) or from a healthy human donor (Hum). All mice were sacrificed on d8, 20 and 60 post-colonization in parallel to age-matched Cv and GF controls. RNA was extracted from ileal tissue, and processed to biotin-labelled cRNA, and then hybridized to the NuGO array (mouse) NuGO_Mm1a520177. Microarray analysis compared gene expression in ileum tissue of all the treatment groups GF, Cv, Cvd, Hum and SFB (N=3 per treatment group per time-point). Data was considered significant when P<0.05 using the Benjamini and Hochberg false discovery method.
2010-05-05 | E-GEOD-18056 | biostudies-arrayexpress
Project description:Microbiota-induced cytokine responses participate in gut homeostasis, but the cytokine balance at steady-state and the role of individual bacterial species in setting the balance remain elusive. Using gnotobiotic mouse models, we provide a systematic analysis of the role of microbiota in the induction of cytokine responses in the normal intestine. Colonization by a whole mouse microbiota orchestrated a broad spectrum of pro-inflammatory (Th1, Th17) and regulatory T cell responses. Unexpectedly, most tested complex microbiota and individual bacteria failed to efficiently stimulate intestinal cytokine responses. A potent cytokine-inducing function was however associated with non-culturable host-specific species, the prototype of which was the Clostridia-related Segmented Filamentous Bacterium, and this bacterial species recapitulated the coordinated maturation of T cell responses induced by the whole mouse microbiota. Our study demonstrates the non-redundant role of microbiota members in the regulation of gut immune homeostasis.
2009-09-11 | GSE18056 | GEO
Project description:To compare the similarities and differences in species diversity of the gut microbiota between the patients with melasma and healthy subjects. The feces were collected for 16S rRNA sequencing analysis of the gut microbiota.
2022-10-25 | GSE214430 | GEO
Project description:Approximately 15% of US adults have circulating levels of uric acid above its solubility limit, which is causally linked to the inflammatory disease gout. In most mammals, uric acid elimination is facilitated by the enzyme uricase. However, human uricase is a pseudogene, having been inactivated early in hominid evolution. Though it has long been known that a substantial amount of uric acid is eliminated in the gut, the role of the gut microbiota in hyperuricemia has not been studied. Here we identify a gene cluster, widely distributed in the gut microbiome, that encodes a pathway for uric acid degradation. Stable isotope tracing demonstrates that gut bacteria metabolize uric acid to xanthine or short chain fatty acids such as acetate, lactate and butyrate. Ablation of the microbiota in uricase-deficient mice causes profound hyperuricemia, and anaerobe-targeted antibiotics increase the risk of gout in humans. These data reveal a role for the gut microbiota in uric acid excretion and highlight the potential for microbiome-targeted therapeutics in hyperuricemia.
2023-06-16 | GSE206419 | GEO
Project description:The gut microbiota is considered the host's "second genome" and is closely associated with the host's physiology. We found that the elimination of gut bacteria suppressed ovarian development in Bactrocera dorsalis. Proteomic analysis revealed significant differences in ovarian protein expression after gut bacteria depletion, with differentially expressed proteins enriched in the proteasome and ubiquitin-related pathway. Moreover, ubiquitination levels were significantly reduced in gut bacteria-depleted females, while Enterobacter hormaechei (EH) supplementation rescued ubiquitination levels. Our findings suggest that ubiquitination serves as a mediator through which gut bacteria regulate ovarian development. By ubiquitin-modified proteomic analysis following gut microbiota manipulation and EH supplementation, we aimed to identify ubiquitination targets critical for ovarian development.
2025-08-01 | PXD066837 |
Project description:In this study we investigated whether gut microbiota profile of Italian healthy volunteers could differ based on their geaographical origin. To this purpose, fecal samples were collected from 31 healthy individuals living in 3 different italian regions (Lombardy, North; Lazio, Center; Apulia, South) and their respective microbiota profiles were analyzed employing 16S metagenomic sequencing method. This study identifies differences in the gut microbiota content and richness among individuals with the same ethnicity coming from three different Italian regions.
2026-01-08 | E-MTAB-8136 | biostudies-arrayexpress
Project description:Advanced age is associated with chronic low-grade inflammation, which is usually referred to as inflammaging. Elderly are also known to have an altered gut microbiota composition. However, whether inflammaging is a cause or consequence of an altered gut microbiota composition is not clear. In this study gut microbiota from young or old conventional mice was transferred to young germ-free mice. Four weeks after gut microbiota transfer immune cell populations in spleen, Peyer’s patches, and mesenteric lymph nodes from conventionalized germ-free mice were analyzed by flow cytometry. In addition, whole-genome gene expression in the ileum was analyzed by microarray. Gut microbiota composition of donor and recipient mice was analyzed with 16S rDNA sequencing. Here we show by transferring aged microbiota to young germ-free mice that certain bacterial species within the aged microbiota promote inflammaging. This effect was associated with lower levels of Akkermansia and higher levels of TM7 bacteria and Proteobacteria in the aged microbiota after transfer. The aged microbiota promoted inflammation in the small intestine in the germ-free mice and enhanced leakage of inflammatory bacterial components into the circulation was observed. Moreover, the aged microbiota promoted increased T cell activation in the systemic compartment. In conclusion, these data indicate that the gut microbiota from old mice contributes to inflammaging after transfer to young germ-free mice.
2018-02-14 | GSE104063 | GEO
Project description:Human gut commensals - Genome sequencing and assembly
| PRJNA931461 | ENA
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