Bacteria
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA474907 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR10608740_1.fastq.gz | Fastqsanger.gz | |||
| SRR10608740_2.fastq.gz | Fastqsanger.gz | |||
| SRR10608741_1.fastq.gz | Fastqsanger.gz | |||
| SRR10608741_2.fastq.gz | Fastqsanger.gz |
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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.
2009-09-11 | GSE18056 | GEO
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:The emerging alphavirus chikungunya virus (CHIKV) has infected millions of people. However, the factors modulating disease outcome remain poorly understood. We show that depletion of the gut microbiota in oral antibiotic-treated or germ-free mice leads to greater CHIKV infection and spread within one day of virus inoculation. Perturbation of the gut microbiota alters TLR7-MyD88 signaling in plasmacytoid dendritic cells (pDCs) and blunts systemic production of type I interferon (IFN). Consequently, circulating monocytes express fewer IFN-stimulated genes and become permissive for CHIKV infection. Reconstitution with a single commensal bacterial species, Clostridium scindens, or its derived metabolite, the bile acid deoxycholic acid, can restore pDC- and MyD88-dependent type I IFN responses to restrict systemic CHIKV infection and transmission back to vector mosquitoes. Thus, commensal gut bacteria modulate antiviral immunity and levels of circulating alphaviruses within hours of infection through a bile acid-pDC-IFN signaling axis, which affects virus dissemination and potentially, epidemic spread 3 biological replicates were processed per time point and group
2020-06-09 | GSE152043 | GEO
Project description:The emerging alphavirus chikungunya virus (CHIKV) has infected millions of people. However, the factors modulating disease outcome remain poorly understood. We show that depletion of the gut microbiota in oral antibiotic-treated or germ-free mice leads to greater CHIKV infection and spread within one day of virus inoculation. Perturbation of the gut microbiota alters TLR7-MyD88 signaling in plasmacytoid dendritic cells (pDCs) and blunts systemic production of type I interferon (IFN). Consequently, circulating monocytes express fewer IFN-stimulated genes and become permissive for CHIKV infection. Reconstitution with a single commensal bacterial species, Clostridium scindens, or its derived metabolite, the bile acid deoxycholic acid, can restore pDC- and MyD88-dependent type I IFN responses to restrict systemic CHIKV infection and transmission back to vector mosquitoes. Thus, commensal gut bacteria modulate antiviral immunity and levels of circulating alphaviruses within hours of infection through a bile acid-pDC-IFN signaling axis, which affects virus dissemination and potentially, epidemic spread
2020-05-13 | GSE150387 | 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: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:The mammalian gastrointestinal tract contains a diverse ecosystem of microbial species collectively making up the gut microbiome. Emerging evidence highlights a critical relationship between gut microbiota and neurocognitive development. Consumption of unhealthy yet palatable dietary factors associated with obesity and metabolic dysfunction (e.g., saturated fat, added sugar) produces microbiota dysbiosis and negatively impacts neurocognitive function, particularly when consumed during early life developmental periods. Here we explore whether excessive early life consumption of added sugars negatively impacts neurocognitive development via the gut microbiome. Using a rodent model of habitual sugar-sweetened beverage (SSB) consumption during the adolescent stage of development, we first show that excessive early life sugar intake impairs hippocampal-dependent memory function when tested during adulthood while preserving other neurocognitive domains. Gut microbiome genomic sequencing analyses reveal that early life SSB consumption alters the abundance of various bacterial populations, including elevations in operational taxonomic units within the genus Parabacteroides (P. distasonis and P. johnsonii) whose abundance negatively correlated with memory task performance. Additional results reveal that in vivo Parabacteroides enrichment of cultured P. distasonis and P. johnsonii bacterial species in adolescent rats severely impairs memory function during adulthood. Hippocampus transcriptome analyses identify gene expression alterations in neurotransmitter synaptic signaling, intracellular kinase signaling, metabolic function, neurodegenerative disease, and dopaminergic synaptic signaling-associated pathways as potential mechanisms linking microbiome outcomes with memory impairment. Collectively these results identify microbiota dysbiosis as a mechanism through which early life unhealthy dietary patterns negatively impact neurocognitive outcomes.
2021-02-25 | GSE150091 | GEO
Project description:We developed a non-invasive ex vivo HT29 cell-based minimal model to fingerprint the mucosa-associated microbiota fraction in humans. HT29 cell-associated fractions were characterized by the universal phylogenetic array platform HTF-Microbi.Array, both in presence or in absence of a TNF-M-NM-1-mediated pro-inflammatory stimulus. A high taxonomical level fingerprint profiling of the mucosa-associated microbiota was performed on a group of 12 breast-fed infants and 6 adults (used as controls). Relative abundance of the bacterial species was assessed by using a so-called HTF-Microbi.Array, based on a ligation detection reaction (LDR) - Univerasal array (UA) assay, capable of correctly identify up to 31 intestinal bacterial groups, covering up to 95% of the human gut microbiota
2013-09-26 | E-GEOD-51177 | biostudies-arrayexpress
Project description:We used 16S V3/V4 region amplification to evaluate the composition of bacteria species in mouse fecal pellets. Fecel pellets were collected from young-adult (12 weeks old) wild type C57Bl/6 mice and aged (72 weeks old) wild type C57Bl/6 mice after 21 days of vehicle or antibiotics treatment (to induce gut microbiota depletion). In one sequencing round, we sequenced a total of 12 different fecal samples (3 young control, 3 aged control, 3 young depleted gut microbiota (ABX) and 3 aged depleted gut microbiota (ABX)). Amplicons were indexed using the Nextera XT Index Kit and pooled into a library for Illumina sequencing.
2020-11-03 | GSE160628 | GEO
Project description:Gut microbiota plays a significant role in shaping gut and systematic immune and huge strain- and species- dependent differences exit. Using in-vitro MLN co-culture models, we want to initially uncover these differences. MLN cells were isolated from C57BL/6 mice and co-cultured with bacterial cells with or without anti-CD3 and anti-CD28 antibodies for three days. After that, IL-10 in cell supernatant was measured and RNA was extracted using Trizol reagent. RNA-seq was performed on Illumina Hiseq X ten. Raw sequenced data were filtered by fastp and clean data were mapped to reference genome (Mus_musculus, GRCm39). Data processing adopted featurecounts in subread, abundance_estimates_to_matirx.pl in Trinity, DEseq and ClusterProfiler. We found that all bacterial species activated the innate immunity response. However, only Akkermansia muciniphila and Clostridium butyricum had cognate T cell antigen and activated adaptive immunity responses even without stimulus.
2022-11-21 | GSE189176 | GEO