Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data of Streptococcus pneumoniae against penicillin

ABSTRACT: The increasing rate of penicillin resistance in S. pneumoniae in the early 1970s has resulted in therapeutic challenges and has prompted the need for alternative therapy in the management of pneumococcal infections. The development of penicillin resistance has been documented to be as a result of altered penicillin binding protein which alters the binding capacity of the drug to the organism. We used microarrays to investigate other genes which may be involved in the development of penicillin resistance in S. pneumoniae and identified classes of genes on the surface of the organism which may contribute to resistance.

ORGANISM(S): Streptococcus pneumoniae Streptococcus pneumoniae TIGR4

PROVIDER: GSE21709 | GEO | 2010/05/13

SECONDARY ACCESSION(S): PRJNA127161

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

Expression data of Streptococcus pneumoniae against penicillin

Project description:The increasing rate of penicillin resistance in S. pneumoniae in the early 1970s has resulted in therapeutic challenges and has prompted the need for alternative therapy in the management of pneumococcal infections. The development of penicillin resistance has been documented to be as a result of altered penicillin binding protein which alters the binding capacity of the drug to the organism. We used microarrays to investigate other genes which may be involved in the development of penicillin resistance in S. pneumoniae and identified classes of genes on the surface of the organism which may contribute to resistance. Strains of S. pneumoniae with varying initial susceptibility to penicillin were selected. These strains were grown to the logarithmic phase before being exposed to subinhibitory concentration of penicillin. RNA was extracted before and after penicillin stress and hybridized on Affymetrix microarrays and represented as either Untreated (before penicillin stress) or treated (after penicillin stress). This was carried out for 3 representative strains; S676, I81, and R98. S, I, and R abbreviates Sensitive, Intermediate and resistant to Penicillin.

2010-05-13 | E-GEOD-21709 | biostudies-arrayexpress

Klebsiella pneumoniae peptide hijacks a Streptococcus pneumoniae permease to subvert pneumococcal growth and colonization

Project description:Treatment of pneumococcal infections is limited by antibiotic resistance and exacerbation of disease by bacterial lysis releasing pneumolysin toxin and other inflammatory factors. We identified a novel peptide in the Klebsiella pneumoniae secretome, which enters Streptococcus pneumoniae via its AmiA-AliA/AliB permease. Subsequent downregulation of genes for amino acid biosynthesis and peptide uptake was associated with reduction of pneumococcal growth in defined medium and human cerebrospinal fluid, irregular cell shape, decreased chain length and decreased genetic transformation. The bacteriostatic effect was specific to S. pneumoniae and Streptococcus pseudopneumoniae with no effect on Streptococcus mitis, Haemophilus influenzae, Staphylococcus aureus or K. pneumoniae. Peptide sequence and length were crucial to growth suppression. The peptide reduced pneumococcal adherence to primary human airway epithelial cell cultures and colonization of rat nasopharynx, without toxicity. We also analysed the effect of peptide on the proteome of S. pneumoniae. We found alteration of the proteome by the peptide with some proteins turned on or off in line with the transcriptomic changes. We therefore identified a peptide with potential as a therapeutic for pneumococcal diseases suppressing growth of multiple clinical isolates, including antibiotic resistant strains, while avoiding bacterial lysis and dysbiosis.

2024-04-08 | PXD050408 | Pride

RNAseq transcriptome analysis of Streptococcus pneumoniae 23F treated with PBT2 and zinc

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

Pivotal Roles for Ribonucleases in Streptococcus pneumoniae Pathogenesis

Project description:RNases perform indispensable functions in regulating gene expression in many bacterial pathogens by processing and/or degrading RNAs. Despite the pivotal role of RNases in regulating bacterial virulence factors, the functions of RNases have not yet been studied in the major human respiratory pathogen Streptococcus pneumoniae (pneumococcus). Here, we sought to determine the impact of two conserved RNases, the endoribonuclease RNase Y and exoribonuclease polynucleotide phosphorylase (PNPase), on the physiology and virulence of S. pneumoniae serotype 2 strain D39. We report that RNase Y and PNPase are essential for pneumococcal pathogenesis as both deletion mutants showed strong attenuation of virulence in murine models of invasive pneumonia. Genome-wide transcriptomic analysis revealed that nearly 200 mRNA transcripts were significantly up-regulated, whereas the abundance of several pneumococcal sRNAs, including the Ccn (CiaR Controlled Noncoding RNA) sRNAs, were altered in the ∆rny mutant relative to the wild-type strain. Additionally, lack of RNase Y resulted in pleiotropic phenotypes that included defects in pneumococcal cell morphology and growth in vitro. In contrast, Dpnp mutants showed no growth defect in vitro, but differentially expressed a total of 40 transcripts including the tryptophan biosynthesis operon genes and numerous 5’-cis-acting regulatory RNAs, a majority of which were previously shown to impact pneumococcal disease progression in mice using the serotype 4 strain TIGR4. Altogether our data suggest that RNase Y exerts a global impact on pneumococcal physiology, while PNPase-mediates virulence phenotypes, likely through sRNA regulation.

2021-09-02 | GSE173392 | GEO

Neuraminidase-exposed galactose promotes Streptococcus pneumoniae biofilm formation during colonization

Project description:Galactose promotes pneumococcal biofilms in vivo 15 mRNA profiles of Streptococcus pneumoniae samples that were grown under different conditions were generated using deep sequencing.

2016-08-04 | E-GEOD-85196 | biostudies-arrayexpress

Chromosome segregation in Streptococcus pneumoniae

2011-06-11 | GSE26839 | GEO

Impact of impaired polyamine biosynthesis on Streptococcus pneumoniae TIGR4 gene expression

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

Identification of a two-component system involved in antimicrobial peptide resistance in Streptococcus pneumoniae

Project description:Two-component regulatory systems (TCS) are one of the most widespread mechanism that bacteria use to sense and respond to environmental changes. In Streptococcus pneumoniae, a total of 13 TCS and one orphan response regulator have been identified and many of them have been linked to pathogenicity. Notably, TCS01 strongly contributed to pneumococcal virulence in several infection models. However, it remains one of the least studied TCS in pneumococci and its functional role is still unclear. In this study, we demonstrate that TCS01 upregulates a BceAB-type ATP-Binding Cassette (ABC) transporter that mediates resistance to several antimicrobial peptides targeting lipid II. Even though Tcs01 and BceAB genes are localized far apart from each other in the genome, disruption of either of them equally sensitized the bacterium to the same antimicrobial peptides. Although it is still poorly understood how S. pneumoniae can switch from a harmless colonizer of the human nasopharynx to a serious pathogen causing a variety of diseases, TCS01 likely contributes to the physiopathology of this organism by cooperating with a BceAB-type transporter to sense and induce resistance to antimicrobial peptides encountered in the human host.

2022-03-22 | MSV000089094 | MassIVE

The cop operon is required for copper homeostasis and contributes to virulence in Streptococcus pneumoniae

Project description:High levels of copper are toxic and therefore bacteria must limit free intracellular levels to prevent cellular damage. In this study, we show that a number of pneumococcal genes are differentially regulated by copper, including an operon encoding a CopY regulator, a protein of unknown function (CupA) and a P1-type ATPase, CopA, which is conserved in all sequenced Streptococcus pneumoniae strains. Transcriptional analysis demonstrated that the cop operon is induced by copper in vitro, repressed by the addition of zinc and is autoregulated by the copper-responsive CopY repressor protein. We also demonstrate that the CopA ATPase is a major pneumococcal copper resistance mechanism and provide the first evidence that the CupA protein plays a role in copper resistance. Our results also show that copper homeostasis is important for pneumococcal virulence as the expression of the cop operon is induced in the lungs and nasopharynx of intranasally infected mice, and a copA(-) mutant strain, which had decreased growth in high levels of copper in vitro, showed reduced virulence in a mouse model of pneumococcal pneumonia. Furthermore, using the copA(-) mutant we observed for the first time in any bacteria that copper homeostasis also appears to be required for survival in the nasopharynx. This SuperSeries is composed of the SubSeries listed below.

2011-07-10 | GSE30415 | GEO

Chromosome segregation in Streptococcus pneumoniae

Project description:Segregation of replicated chromosomes during cell division is an essential process in all organisms. Chromosome segregation is promoted by the action of the DNA-binding ParB protein in the rod-shaped model bacterium Bacillus subtilis. How oval shaped bacteria, such as the human pathogen Streptococcus pneumoniae, efficiently segregate their chromosomes is poorly understood. Here, we show that the pneumococcal homolog of ParB is enriched at four centromere-like DNA sequences (parS sites) that are present near the origin of replication. Amplified ChIP DNA was fluorescently labelled using the BioPrime Total Genomic Labeling kit from Invitrogen. Eluate DNA was labelled with AlexA Fluor 3 and input DNA with Alexa Fluor 5. Labelled DNA was hybridized to a DNA-microarray containing amplicons of all open reading frames of S. pneumoniae (Kloosterman et al., 2006).

2011-06-11 | E-GEOD-26839 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data