Streptococcus pneumoniae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA60105 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Streptococcus pneumoniae multi-isolate
| PRJNA51599 | ENA
Project description:The polyamine biosynthesis gene, speE, in Streptococcus pneumoniae TIGR4 is necessary for survival in murine models of pneumococcal pneumonia. To date, there is no description of polyamine biosynthesis dependent pneumococcal gene expression. In this study, we compared gene expression between the wild-type and biosynthesis deficient (speE) TIGR4 by RNA-Seq analysis.
2023-01-01 | E-MTAB-6070 | biostudies-arrayexpress
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: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:<p><em>Streptococcus pneumoniae</em> 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 generates a variety of antimicrobial agents to control infection including zinc stress. Here, we characterized the impact of zinc intoxication on <em>S. pneumoniae</em>, revealing disruptions in central carbon metabolism, lipid biogenesis and peptidoglycan biosynthesis. Characterization of the pivotal peptidoglycan biosynthetic enzyme GlmU revealed an exquisite sensitivity to zinc inhibition. Disruption of the sole zinc efflux pathway, czcD, rendered <em>S. pneumonia</em>e highly susceptible to β-lactam antibiotics. To dysregulate zinc homeostasis in the wild-type strain, we investigated the safe-for-human use ionophore PBT2. PBT2 rendered wild-type <em>S. pneumoniae</em> strains sensitive to a range of antibiotics. Using an invasive ampicillin-resistant strain, we demonstrate in a murine pneumonia infection model the efficacy of PBT2+ampicillin treatment. These findings present a therapeutic modality to break resistance of drug-resistant <em>S. pneumoniae</em>.</p>
2022-02-23 | MTBLS318 | MetaboLights
Project description:This study reports on the co-administration of a zinc ionophore (PBT-2) and ampicillin to break antibiotic resistance of Streptococcus pneumoniae in a murine pneumonia model. The molecular mechanism for this heightened antimicrobial activity was identified through transcriptomic and metabolomic analyses of a wild type strain and a zinc efflux mutant to identify cellular targets of zinc intoxication. This revealed that zinc intoxication induces numerous cellular disruptions, which when combined with frontline antibiotics, can break antibiotic resistance and potentially preclude further resistance from emerging.
2022-02-01 | GSE159901 | GEO
Project description:Streptococcus pneumoniae normally resides in the human nasopharynx in a non-disease state. In response to yet unknown triggers it can descend to the lower respiratory tract and/or invade the bloodstream. Regulation and activation of virulence genes play essential roles in this process of disease development. A putative transcriptional regulator in S. pneumoniae, MgrA, with homology to a virulence gene activator, mga, of Group A streptococcus (GAS) was previously identified as being required for development of pneumonia in a murine model. In this work we confirm that mgrA is required for both nasopharyngeal carriage and pneumonia. Transcriptional profiling by microarray technology through the growth course of a strain that bears a deletion of mgrA (AC1500) with that of a strain that over expresses Mgra (AC1481) is used to show that MgrA acts as a repressor of the previously characterized rlrA pathogenicity islet. This is manifested phenotypically by a decrease in adherence to epithelial cells in tissue culture since rlrA pathogenicity islet contains genes mediating adherence.
2005-07-21 | E-SMDB-2166 | biostudies-arrayexpress
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:Diagnostic primer extension assay to serotype Streptococcus pneumoniae. Assay validation. Background: Monitoring of Streptococcus pneumoniae serotype epidemiology is essential since serotype replacement is a concern when introducing new polysaccharide-conjugate vaccines. To simplify S. pneumoniae serotyping, a novel PCR-based automated microarray assay was developed to assist in the tracking of the serotypes. Results: Autolysin (lytA), pneumolysin (ply) and eight genes located in the capsular operon (cps) were amplified using multiplex PCR. This step was followed by a tagged fluorescent primer extension step targeting serotype-specific polymorphisms. The tagged primers were then hybridized to a microarray. Results were exported to an expert system that transforms genetic typing data into capsular serotype identification. The assay was validated on 166 cultured S. pneumoniae samples from 63 different serotypes as determined by the Quellung method. In addition, the assay was tested on clinical specimens including 43 cerebrospinal fluid samples from patients with meningitidis and 59 nasopharyngeal aspirates from bacterial pneumonia patients. The assay presented with no cross-reactivity for 24 relevant bacterial species found in these types of samples. The limit of detection for serotyping and S. pneumoniae detection was 100 genome equivalent per reaction. Conclusion: This automated assay is amenable to clinical testing and does not require any culturing of the samples. The assay will be useful for the evaluation of serotype prevalence changes after new conjugate vaccines introduction.
2013-12-31 | GSE45865 | GEO