Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1148144 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30267103_1.fastq.gz | Fastqsanger.gz | |||
| SRR30267103_2.fastq.gz | Fastqsanger.gz | |||
| SRR30267106_1.fastq.gz | Fastqsanger.gz | |||
| SRR30267106_2.fastq.gz | Fastqsanger.gz | |||
| SRR30260809_1.fastq.gz | Fastqsanger.gz |
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Project description:The use of microbiological cultures for diagnosing bacterial infections in young febrile infants have substantial limitations, including false positive and false negative cultures, and non-ideal turn-around times. Analysis of host genomic expression patterns (“RNA biosignatures”) in response to the presence of specific pathogens, however, may provide an alternate and potentially improved diagnostic approach. This study was designed to define bacterial and non-bacterial RNA biosignatures to distinguish these infections in young febrile infants.
2016-07-27 | GSE64456 | GEO
Project description:The use of microbiological cultures for diagnosing bacterial infections in young febrile infants have substantial limitations, including false positive and false negative cultures, and non-ideal turn-around times. Analysis of host genomic expression patterns (âRNA biosignaturesâ) in response to the presence of specific pathogens, however, may provide an alternate and potentially improved diagnostic approach. This study was designed to define bacterial and non-bacterial RNA biosignatures to distinguish these infections in young febrile infants. A total of 279 febrile infants and 19 healthy afebrile control infants aged 0-6 months (for a total of 298 samples) for microarray analysis. For analytic purposes, we classified patients into two groups, those with bacterial infections (n=89) and those with non-bacterial infections (n=190). 144 of the samples were run on Illumina HT12 V4 R1 chips. Of these, there were 34 bacterial infections, 105 non-bacterial infections, and 5 healthy afebrile controls. 154 of the samples were run on Illumina HT12 V4 R2 chips. Of these, there were 55 bacterial infections, 85 non-bacterial infections, and 14 healthy afebrile controls.
2016-07-27 | E-GEOD-64456 | biostudies-arrayexpress
Project description:Group B Streptococcus (GBS) is a leading cause of infant sepsis worldwide. Colonization of the gastrointestinal tract is a critical precursor to late-onset disease in exposed newborns. Neonatal susceptibility to GBS intestinal translocation stems from intestinal immaturity; however, the mechanisms by which GBS exploits the immature host remain unclear. β-hemolysin/cytolysin (βH/C) is a highly conserved toxin produced by GBS capable of disrupting epithelial barriers. However, its role in the pathogenesis of late-onset GBS disease is unknown. Our aim was to determine the contribution of βH/C to intestinal colonization and translocation to extraintestinal tissues. Using our established mouse model of late-onset GBS disease, we exposed animals to GBS COH-1 (WT), a βH/C-deficient mutant (KO), or vehicle control (PBS) via gavage. Blood, spleen, brain, and intestines were harvested 4 days post-exposure for determination of bacterial burden and isolation of intestinal epithelial cells. We used RNA-sequencing to examine the transcriptomes and performed gene ontology enrichment and KEGG pathway analysis. A separate cohort of animals were followed longitudinally to compare colonization kinetics and mortality between WT and KO groups. We demonstrate that disseminated to extraintestinal tissues occurred only in the WT exposed animals. We observed major transcriptomic changes in the colon of colonized animals, but not in the small intestine. We noted differential expression of genes among WT and KO exposed mice indicating that βH/C contributes to alterations in epithelial barrier structure and immune response signaling. Overall, our results demonstrate an important role for βH/C in the pathogenesis of late-onset GBS disease.
2023-05-31 | GSE230856 | GEO
Project description:Transcription profiling by array of children blood with serious bacterial infections
2025-01-22 | E-MEXP-3567 | ExpressionAtlas
Project description:Gut-resident microbes contribute to host health via multiple mechanisms. Some of the most striking gut microbiota induced effects occur in the extraintestinal tissues and are restricted to early life. The mechanisms by which gut residing bacteria induce effects on distant host tissues and why this is restricted to a period in early life are largely unknown. We found that a subset of live gut-resident bacteria spontaneously translocate from gut to extraintestinal tissues in preweaning, but not adult mice. Translocation in preweaning mice appeared physiologic as it did not induce an inflammatory response and was in part controlled by sphingosine-1-phsophate receptor (S1PR) expressing host cells and host goblet cells. One translocating strain, Lactobacillus animalisWU, contained unique coding sequences for genes in the tyrocidine-gramicidin antibiotic-synthesizing gene cluster as well as five other regions putatively producing secondary metabolites with anti-microbial activity. Lactobacillus animalisWU exhibited antimicrobial activity against the late-onset sepsis pathogen E. coli ST69 in vitro, and translocation of L. animalisWU protected preweaning mice from systemic E. coli ST69 sepsis in vivo. These observations demonstrate a previously unappreciated higher-level symbiosis with our gut microbes.
2025-04-02 | GSE278303 | GEO
Project description:Extraintestinal pathogenic Escherichia coli (ExPEC) is a common bacterial strain causing diverse diseases in humans and animals. To analyse the detailed mechanisms underlying ExPEC-mediated sepsis in humans, the transcriptome response of mice at 3h,6h, and 12h after ExPEC infection was analyzed by RNA-seq of mouse spleen samples.
2022-11-11 | GSE140637 | GEO
Project description:HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of PBMCs from HOIL-1- and MYD88-deficient patients.
2012-10-28 | GSE40838 | GEO
Project description:Background: Distinguishing between bacterial and viral lower respiratory tract infections (LRTI) in hospitalized patients remains challenging. Transcriptional profiling is a promising tool for improving diagnosis in LRTI. Methods: We performed whole blood transcriptional analysis in a cohort of 118 adult patients (median [IQR] age, 61 [50-76] years) hospitalized with bacterial, viral or viral-bacterial LRTI, and 40 age-matched healthy controls (60 [46-70] years). We applied class comparisons, modular analysis and class prediction algorithms to identify distinct biosignatures for bacterial and viral LRTI, which were validated in an independent group of patients. Results: Patients were classified as bacterial (B, n=22), viral (V, n=71) and bacterial-viral LRTI (BV, n=25) based on comprehensive microbiologic testing. Compared with healthy controls statistical group comparisons (p<0.01; with multiple test corrections) identified 3,376 differentially expressed genes in patients with B-LRTI; 2,391 in V-LRTI, and 2,628 in BV-LRTI. Independent of etiologic pathogen, patients with LRTI demonstrated overexpression of innate immunity and underexpression of adaptive immunity genes. Patients with B-LRTI showed significant overexpression of inflammation (B>BV>V) and neutrophils (B>BV>V) while those with V-LRTI displayed significantly greater overexpression of interferon genes (V>BV>B). The K-Nearest Neighbors (K-NN) algorithm identified 10 classifier genes that discriminated patients with bacterial vs viral LRTI with 97% [95%CI: 84-100] sensitivity and 92% [77-98] specificity. In comparison, procalcitonin classified bacterial vs viral LRTI with 38% [18-62] sensitivity and 91% [76-98] specificity. Conclusions: Transcriptional profiling can be used as a helpful tool for the diagnosis of adults hospitalized with LRTI. 158 samples, no replicates; bacterial LRTI n=22, viral LRTI n=71, bacterial-viral coinfections n=25, and healthy controls n=40
2015-09-14 | E-GEOD-60244 | biostudies-arrayexpress
Project description:Defining RNA Transcriptional Biosignatures to Distinguish Febrile Infants 60 Days of Age and Younger with Bacterial vs Non-Bacterial Infections
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Project description:HOIL-1 deficient disease is a new early onset fatal autosomal recessive human disorder charaterized by chronic auto-inflammation, recurrent invasive bacterial infections and progressive muscular amylopectinosis. We studied the effect of TNF-α and IL-1β on transcriptional changes of primary fibroblasts from HOIL-1-, MYD88- and NEMO-deficient patients.
2012-10-28 | GSE40560 | GEO