Ontology highlight
ABSTRACT:
PROVIDER: PRJNA799655 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17710000.fastq.gz | Fastqsanger.gz | |||
| SRR17710001.fastq.gz | Fastqsanger.gz | |||
| SRR17710002.fastq.gz | Fastqsanger.gz | |||
| SRR17710003.fastq.gz | Fastqsanger.gz | |||
| SRR17710004.fastq.gz | Fastqsanger.gz |
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Project description:Acute respiratory infections (ARI), which generally begin with colonization of the mucosal surfaces of the upper respiratory tract (URT), are a leading cause of morbidity and mortality with the highest rate in infants. As a common colonizer of the URT, and one of the most prevalent causes of life-threatening infections in the pediatric population, Streptococcus pneumoniae (Spn) was used as a model pathogen to investigate the effect of age during URT infection. We used RNA-sequencing to transcriptionally profile and compare the mucosal epithelia of infant and adult mice at baseline (mock-infected) and during Spn infection. Analysis of the screen revealed an age-dependent alteration of genes involved in mucosal defense mechanisms that included dampened expression of ubiquitous antimicrobial molecules and tight junction proteins in infant mice compared to adults. These results demonstrate a window of vulnerability during postnatal development when altered mucosal barrier function may facilitate bacterial colonization and invasion.
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Project description:Streptococcus pneumoniae (Spn) is the predominant causative organism of acute otitis media (AOM) in children. A human cDNA microarray comprising 30,968 human genome probes was used to evaluate the transcriptional changes that occur in peripheral blood mononuclear cells (PBMC) at the onset of clinical AOM caused by Spn infection in children after comparison of microarray results with the pre-infection healthy stage of the same children.
2010-07-26 | GSE23140 | GEO
Project description:Aging is associated with declining immunity and inflammation as well as alterations in the gut microbiome with a decrease of beneficial microbes and increase in pathogenic ones. The aim of this study was to investigate aging associated gut microbiome in relation to immunologic and metabolic profile in a non-human primate (NHP) model. 12 old (age>18 years) and 4 young (age 3-6 years) Rhesus macaques were included in this study. Immune cell subsets were characterized in PBMC by flow cytometry and plasma cytokines levels were determined by bead based multiplex cytokine analysis. Stool samples were collected by ileal loop and investigated for microbiome analysis by shotgun metagenomics. Serum, gut microbial lysate and microbe-free fecal extract were subjected to metabolomic analysis by mass-spectrometry. Our results showed that the old animals exhibited higher inflammatory biomarkers in plasma and lower CD4 T cells with altered distribution of naïve and memory T cell maturation subsets. The gut microbiome in old animals had higher abundance of Archaeal and Proteobacterial species and lower Firmicutes than the young. Significant enrichment of metabolites that contribute to inflammatory and cytotoxic pathways was observed in serum and feces of old animals compared to the young. We conclude that aging NHP undergo immunosenescence and age associated alterations in the gut microbiome that has a distinct metabolic profile.
2022-02-01 | E-MTAB-10160 | biostudies-arrayexpress
Project description:D’Mello et al. detail host-pathogen interaction gene expression profiles of Streptococcus pneumoniae (Spn) and its infected host at disease relevant anatomical sites using mice as experimental models. The authors identify the core and organ-specific transcriptomes of Spn, show that bacterial and host gene expression profiles are highly distinct during asymptomatic colonization versus disease-causing infection, and demonstrate that Spn and host genes with high levels of expression contribute to pathogenesis or host defense, respectively.
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Project description:The objectives of the study were to examine the gene expression profile of human pleural mesothelial cells following infection with Streptococcus pneumoniae. The abstract is as follows: Streptococcus pneumoniae (Spn) is a major causative organism of empyema, an inflammatory condition occurring in the pleural sac. In this study, we used human and Spn cDNA microarrays to characterize the transcriptional responses occurring during initial contact between Spn and a human pleural mesothelial cell line (PMC) in vitro. Using stringent filtering criteria, 42 and 23 Spn genes were up-and down-regulated respectively. In particular, genes encoding factors potentially involved in metabolic processes and Spn adherence to eukaryotic cells were up-regulated e.g. glnQ, glnA, aliA, PsaB, LytB and nox. After Spn initial contact, 870 human genes were differentially regulated and the largest numbers of significant gene expression changes were found in canonical pathways for eukaryotic initiation factor 2 signaling (60 genes out of 171), oxidative phosphorylation (32/103), mitochondrial dysfunction (37/164), eIF4 and p70S6K signaling (28/142), mTOR signaling (27/182), NRF2-mediated oxidative stress response (20/177), epithelial adherens junction remodeling (11/66) and ubiquitination (22/254). The cellular response appeared to be directed towards host cell survival and defense. Spn did not activate NF-kB or phosphorylate p38 MAPK or induce cytokine production. Moreover, Spn infection of TNF-α pre-stimulated PMC inhibited production of IL-6 and IL-8 secretion by >50% (p<0.01). In summary, his descriptive study provides datasets and a platform for examining further the molecular mechanisms underlying the pathogenesis of empyema.
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Project description:Systemic infection induces conserved physiological responses that include both resistance and ‘tolerance of infection’ mechanisms. Among these responses, temporary anorexia associated with an infection is often beneficial. It poses, however, a problem for the trillions of microbes residing in the gastrointestinal tract, as they also experience reduced substrate availability. We hypothesized that under anorectic conditions caused by infection, the host might activate protective mechanisms to support the gut microbiota during the acute phase of the disease. Here, we report that systemic exposure to Toll-like receptor (TLR) ligands causes rapid α1,2-fucosylation of the small intestine epithelial cells (IEC). The process requires sensing of TLR agonists and production of IL-23 by dendritic cells, activation of innate lymphoid cells and expression of α1,2-Fucosyltransferase-2 (Fut2) by IL-22-stimulated IECs. Fucosylated proteins are shed into the lumen and fucose is utilized by microbiota, as shown using reporter bacteria and by transcriptional profiling of the gut microbiome. Fucosylation also reduces the expression of bacterial virulence genes within the commensal gut microbiome and improves host tolerance of the mild pathogen Citrobacter rodentium. Thus, rapid IEC fucosylation appears to be a protective mechanism that utilizes the host’s resources to maintain host-microbial interactions during pathogen-induced stress. RNA-Seq analysis of the murine gut microbiome following LPS exposure. Fut2-/- (B6.129X1-Fut2tm1Sdo/J) mice were backcrossed greater than 7 generations to BALB/c. Fut2-/- (KO) and Fut2+/- (Het) animals were analyzed.
2014-10-24 | E-GEOD-60874 | biostudies-arrayexpress
Project description:Today, swine is regarded as promising biomedical model, however, its gastrointestinal microbiome dynamics have been less investigated than that of humans or murine models . The aim of this study was to establish a high-throughput multi-omics pipeline to investigate the healthy fecal microbiome of swine and its temporal dynamics as basis for future infection studies. To this end, a homogenization protocol based on deep-frozen feces followed by integrated sample preparation for different meta-omics analyses was developed. Subsequent data integration linked microbiome composition with function, i.e. expressed proteins and secreted metabolites.
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