Streptococcus pneumoniae
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR121414_1.fastq.gz | Fastqsanger.gz | |||
| DRR121414_2.fastq.gz | Fastqsanger.gz | |||
| DRR121415_1.fastq.gz | Fastqsanger.gz | |||
| DRR121415_2.fastq.gz | Fastqsanger.gz | |||
| DRR121416_1.fastq.gz | Fastqsanger.gz |
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Project description:For the last two decades, the three most common causes of death world-wide have been ischemic heart disease, cerebrovascular disease and respiratory tract infections; the latter being caused mainly by the influenza virus and the bacterial pathogen Streptococcus pneumoniae (Spn). Reports through this period of time have shown that elderly patients admitted to the hospital for severe community-acquired pneumonia (CAP), experience ~10-25% mortality rates and up to 40% of them expired within one year. A key contributing factor for the observed high mortality rate are the major adverse cardiac events (MACE) that occur during hospitalization and convalescence9. Notably, during severe pneumococcal infections, Spn, the most common cause of CAP, has been shown to be capable of myocardial invasion, induction of cardiomyocyte death, and disruption of cardiac contractility. In addition, changes to heart functionality have also been reported after influenza infection in humans, however the mechanisms for this remain unclear.
2021-12-23 | PXD016137 | Pride
Project description:Streptococcus (S.) pneumoniae is the most frequently isolated causative pathogen community-acquired pneumonia, a leading cause of mortality worldwide. We investigated the role of the inflammasome sensor NLRP3 and the inflammasome adapter ASC during S. pneumoniae pneumonia. Detailed analysis of the early inflammatory response in the lung by whole genome transcriptional profiling, we identified several mediators that were differentially expressed between Nlrp3-/- and Asc-/ - mice. WT, Nlrp3- and Asc-deficient mice were intranasally inocculated with Streptococcus pneumoniae D39 and ATCC6303 both at high and low dose. Lung homogenates were harvested and gene expression profiling was performed.
2014-11-27 | E-GEOD-42464 | biostudies-arrayexpress
Project description:Streptococcus (S.) pneumoniae is the most frequently isolated causative pathogen community-acquired pneumonia, a leading cause of mortality worldwide. We investigated the role of the inflammasome sensor NLRP3 and the inflammasome adapter ASC during S. pneumoniae pneumonia. Detailed analysis of the early inflammatory response in the lung by whole genome transcriptional profiling, we identified several mediators that were differentially expressed between Nlrp3-/- and Asc-/ - mice.
2014-12-15 | GSE42464 | GEO
Project description:Streptococcus pneumoniae is the leading cause of community-acquired pneumonia. The release of the pore-forming cholesterol-dependent cytolysin (CDC) pneumolysin (PLY) and hydrogen peroxide (H2O2), a physiological metabolite, is an important virulence determinant of pneumococci.
2023-08-09 | GSE240442 | GEO
Project description:Pneumonia caused by Streptococcus pneumoniae is a leading cause of death worldwide, and bacterial resistance to antimicrobial drugs has become a major issue. A growing body of evidence indicates that the successful treatment of bacterial infections results from synergy between antibiotic-mediated direct antibacterial activity and the host’s immune defenses. However, the mechanisms underlying the protective immune responses induced by amoxicillin (a β-lactam antibiotic used as the first-line treatment of S. pneumoniae infections) have not been characterized. A better understanding of amoxicillin’s effects on host-pathogen interactions might facilitate the development of other treatment options. Given the crucial role of neutrophils in the control of S. pneumoniae infections, we decided to investigate amoxicillin’s impact on neutrophil development in a mouse model of pneumococcal superinfection. Although a single therapeutic dose of amoxicillin prevented local and systemic inflammatory responses, it did not impair the emergency granulopoiesis triggered in the bone marrow by S. pneumoniae. Importantly, treatment of pneumonia with amoxicillin was associated with a greater mature neutrophil count in the bone marrow; these neutrophils had specific transcriptomic and proteomic profiles. Furthermore, amoxicillin-conditioned, mature neutrophils in the bone marrow had a less activated phenotype and might be rapidly mobilized in peripheral tissues in response to systemic inflammation. Thus, by revealing a novel effect of amoxicillin on the development and functions of bone marrow neutrophils during Streptococcus pneumoniae pneumonia, our findings provide new insights into the impact of amoxicillin treatment on host immune responses.
2023-10-09 | PXD042496 | Pride
Project description:Infections by Streptococcus pneumoniae are a major cause of morbidity and mortality worldwide, often causing community-acquired pneumonia, otitis media and also bacteremia and meningitis. Studies on S. pneumoniae are mainly focused on its virulence or capability to evade the host immune system, but little is known about the injury caused in lungs during a pneumococcal infection. Herein we compared the proteome profile of lungs from S. pneumoniae-infected mice with control mice by means of DIGE technology. In order to obtain reliable results three biological replicas were used, and four technical replicas were carried out for each biological replica. Proteomic comparison was performed at two time points: 24 and 48 hours post infection. A total of 91 proteins were identified with different abundance. We found important changes in the protein profiles during pneumococcal infection mainly associated with regulation of vesicle-mediated transport, wound healing, and cytoskeleton organization. In conclusion, S. pneumoniae may manipulate cytoskeleton of the cell during a lung infection likely by the death of eukaryotic cells.
2018-06-10 | PXD006393 | Pride
Project description:Draft genome sequences of Streptococcus pneumoniae strains from cluster infections in Niigata, Japan
| PRJDB8666 | ENA
Project description:Draft genome sequences of Streptococcus pneumoniae isolated from Japan
| PRJDB10994 | ENA
Project description:Streptococcus pneumoniae is the primary cause of community-acquired bacterial pneumonia with rates of penicillin and multi-drug resistance exceeding 80% and 40%, respectively. The innate immune response uses various chemical insults to control infection, including metal stress mediated by localized changes in zinc abundance. Here, we characterized the impact of S. pneumoniae zinc intoxication revealing disruptions in central carbon metabolism, lipid biogenesis and peptidoglycan biosynthesis. To dysregulate zinc homeostasis in the wild-type strain, we investigated the safe-for-human use ionophore PBT2. PBT2 rendered wild-type S. pneumoniae strains sensitive to a range of antibiotics.
2021-10-01 | GSE160372 | 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