Ontology highlight
ABSTRACT:
PROVIDER: PRJNA971933 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24577500_1.fastq.gz | Fastqsanger.gz | |||
| SRR24577500_2.fastq.gz | Fastqsanger.gz | |||
| SRR24577501_1.fastq.gz | Fastqsanger.gz | |||
| SRR24577501_2.fastq.gz | Fastqsanger.gz | |||
| SRR24577502_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 356 |
Similar Datasets
Project description:Denture plaque microbial composition and aspiration pneumonia, any risk in older patient: an observational study
| PRJNA913487 | ENA
Project description:This project was a prospective translational study aimed at evaluating gene expression profiles (GEP) of patients with ventilator-associated pneumonia (VAP) . GEP of VAP were compared with a control group of patients which did not developed ventilator-associated lower respiratory tract infection despite being subjected to mechanical ventilation.
2018-01-31 | E-MTAB-5638 | biostudies-arrayexpress
Project description:Introduction: Diagnosis of severe influenza pneumonia remains challenging because of the lack of correlation between presence of influenza virus and patient’s clinical status. We conducted gene expression profiling in the whole blood of critically ill patients to identify a gene signature that would allow clinicians to distinguish influenza infection from other causes of severe respiratory failure (e.g. bacterial pneumonia, non-infective systemic inflammatory response syndrome). Methods: Whole blood samples were collected from critically ill individuals and assayed on Illumina HT-12 gene expression beadarrays. Differentially expressed genes were determined by linear mixed model analysis and over-represented biological pathways determined using GeneGo MetaCore. Results: The gene expression profile of H1N1 influenza A pneumonia was distinctly different from bacterial pneumonia and systemic inflammatory response syndrome. The influenza gene expression profile is characterized by up-regulation of genes from cell cycle regulation, apoptosis and DNA-damage response pathways. In contrast, no distinctive gene-expression signature was found in patients with bacterial pneumonia or systemic inflammatory response syndrome. The gene expression profile of influenza infection persisted through five days of follow-up. Furthermore, in patients with primary H1N1 influenza A infection who subsequently developed bacterial co-infection, the influenza gene-expression signature remained unaltered, despite the presence of a super-imposed bacterial infection. Conclusions: The whole blood expression profiling data indicates that the host response to influenza pneumonia is distinctly different from that caused by bacterial pathogens. This information may speed up identification of the cause of infection in patients presenting with severe respiratory failure, allowing appropriate patient care to be undertaken more rapidly. Daily PAXgene samples for up to 5 days for; influenza A pneumonia patients (n=8), bacterial pneumonia patients (n=16), mixed bacterial and influenza A pneumonia patients (n=3), systemic inflammatory response patients (SIRS, n=13). Days 1 and 5 PAXgene samples for healthy control individuals
2012-08-14 | E-GEOD-40012 | biostudies-arrayexpress
Project description:Rhinovirus (RV) is the most prevalent human respiratory virus. Each year, RV infects billions of people and is responsible for at least half of all common colds, the most common illness of humans. RV infection also affects the morbidity of a range of respiratory illnesses, such as bronchiolitis, pneumonia, asthma, chronic obstructive pulmonary disease, and cystic fibrosis. Despite its biological importance and public health significance, little is known about the genetic architecture of response to RV. To address this, we obtained genome-wide genotype and gene expression data in uninfected and RV-infected peripheral blood mononuclear cells (PBMCs) from 98 individuals. We characterized gene expression differences in response to RV infection and mapped expression quantitative trait loci (eQTLs) in both uninfected and RV-infected PBMCs.
2015-04-14 | GSE53543 | GEO
Project description:Rationale: Streptococcus pneumoniae is the most common bacterial cause of community acquired pneumonia. Some clinical trials have demonstrated a beneficial effect of corticosteroid therapy in community acquired pneumonia, but the mechanisms of this benefit remain unclear. Objectives: To investigate the biologic effects of corticosteroids in pneumococcal pneumonia in mice and in patients Methods: We studied lower respiratory tract transcriptomes from an observational cohort of mechanically ventilated patients and from a pneumonia model in mice. We also carried out comprehensive physiologic, biochemical, and histological analyses in mice to identify mechanisms of lung injury in S. pneumoniae with and without adjunctive steroid therapy. Measurement and Main Results: Transcriptomic analysis identified pleiotropic effects of steroid therapy on the lower respiratory tract in critically ill patients with pneumococcal pneumonia, findings that were reproducible in mice. In mice with pneumonia, dexamethasone in combination with ceftriaxone reduced (1) pulmonary edema formation, (2) alveolar protein permeability, (3) proinflammatory cytokine release, (4) histopathology lung injury score, and (5) hypoxemia, but did not increase bacterial burden. Conclusions: In combination with appropriate antibiotics in mice, treatment of pneumococcal pneumonia with steroid therapy reduces hypoxemia, pulmonary edema, lung permeability, and histologic criteria of lung injury, and also altered inflammatory responses at the protein and gene expression level. The concordance of transcriptional data in the mouse model and in patients with pneumococcal pneumonia supports the translational relevance of this work.
2024-06-05 | GSE246398 | GEO
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036014 | Pride
Project description:With annually 2.56 million deaths worldwide, pneumonia is one of the leading causes of death. Most frequent causative pathogens are Streptococcus pneumoniae and influenza A virus. Lately, the interaction between pathogens, the host and its microbiome gained more attention. A healthy microbiome is known to enhance the immune response towards pathogens, however, our knowledge on how infections affect the microbiome is still scarce. In this study, a meta-omics approach was used to investigate the impact of S. pneumoniae and influenza A virus infection on structure and function of the respiratory and gastrointestinal microbiomes of mice. In particular, the taxonomic composition of the respiratory microbiome was less affected by bacterial colonization and viral infection compared to S. pneumoniae infection. Pneumococcal pneumonia led to reduction of bacterial families and lower diversity in the respiratory microbiome, whereas diversity/richness was unaffected following H1N1 infection. Within the gastrointestinal microbiome we found exclusive changes in structure and function depending on the pneumonia inducing pathogen. Exemplarily, increased abundance of Akkermansiaceae and Spirochaetaceae, as well as decreased amounts of Clostridiaceae in response to S. pneumoniae infection, while increased presence of Enterococcaceae and Staphylococcaceae was specific for viral-induced pneumonia. Investigation of the intestinal microbiomes functional composition revealed reduced expression of flagellin and rubrerythrin and increased levels of ATPase during pneumococcal infection, while increased amounts of acetyl-CoA acetyltransferase and, enoyl-CoA transferase were unique after H1N1 infection. The identification of specific taxonomical and functional profiles during infection with a respective pathogen could deliver new insights in the role of the microbiome during disease and be beneficial for discrimination of pneumococcal- or viral-induced pneumonia.
2023-03-24 | PXD036129 | Pride