E-MTAB-7841
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-7841 | ExpressionAtlas | 2019-09-09
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:RNAseq of human epithelial nasopharyngeal carcinoma cell line Detroit 562, following infection with strains of Streptococcus pneumoniae
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Project description:The transcriptomic innate immune response derived from human nasal epithelial cells depends on how Streptococcus pneumoniae colonises the nasopharynx. This study compared three wild type strains and one deficient in pneumolysin to explore the pathways of epithelial activation following a three hour infection in vitro.
2019-05-01 | E-MTAB-7841 | biostudies-arrayexpress
Project description:Human bronchial epithelial cell line Beas-2B were infected with Streptococcus pneumoniae at Multiplicity of Infection (MOI) of 0.5 and 1 or treated with lipoteichonic acid (LTA) for 9 and 16 h. The mRNA profile changes upon infection shall be determined to investigate Streptococci pathogenesis.
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Project description:Multiscale mathematical model of pneumococcal alveolar infection. This model analyses the role of cellular and molecular interactions during the first 10 h after alveolar invasion of Streptococcus pneumoniae bacteria. By “multi-level” we mean that we simulated the interplay between different temporal and spatial scales in a single computational model. In this instance, we included the intracellular scale of processes driving lung epithelial cell activation together with the scale of cell-to-cell interactions between bacteria and alveolar macrophages at the alveolar tissue. The model combines agent-based modelling and ODE modelling strategies. The original article of the article can be found in https://doi.org/10.3389/fcimb.2018.00159.
2018-11-14 | MODEL1805170001 | BioModels
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
Project description:Mouse lung RNAseq after infection with Influenza A virus (H1N1, PR/8/34, mouse-adapted) and Streptococcus pneumoniae (serotype 19F, strain BHN 100) Results: Differentially expressed genes were observed after single and co-infection Project: COST_mouse_2021_lung
2022-08-31 | GSE196708 | GEO
Project description:Rationale: Respiratory syncytial virus (RSV) and Streptococcus pneumoniae are major respiratory pathogens. Co-infection with RSV and S. pneumoniae is associated with severe and often fatal pneumonia but the molecular basis for this remains unclear. Objectives: To determine if interaction between RSV and pneumococci enhances pneumococcal virulence. Methods: We used confocal microscopy and western blot to identify the receptors involved in direct binding of RSV and pneumococci, the effects of which were studied in both in vivo and in vitro models of infection. Human ciliated respiratory epithelial cell cultures were infected with RSV for 72h and then challenged with pneumococci. Pneumococci were collected after 2h exposure and changes in gene expression determined using qRT-PCR. Results: Following incubation with RSV or purified G protein, pneumococci demonstrated a significant increase in the inflammatory response and bacterial adherence to human ciliated epithelial cultures and markedly increased virulence in a pneumonia model in mice. This was associated with extensive changes in the pneumococcal transcriptome and significant upregulation in the expression of key pneumococcal virulence genes, including the gene for the pneumococcal toxin, pneumolysin. We show that mechanistically this is due to RSV G glycoprotein binding penicillin binding protein 1a. Conclusion: The direct interaction between a respiratory virus protein and the pneumococcus resulting in increased bacterial virulence and worsening disease outcome is a new paradigm in respiratory infection. Comparison of the Streptococcus pneumoniae D39 RSV treated compared to BSA Treated in BEBM medium One condition design comparision of two strains including a dye swap
2014-06-21 | E-GEOD-58425 | biostudies-arrayexpress
Project description:Rationale: Respiratory syncytial virus (RSV) and Streptococcus pneumoniae are major respiratory pathogens. Co-infection with RSV and S. pneumoniae is associated with severe and often fatal pneumonia but the molecular basis for this remains unclear. Objectives: To determine if interaction between RSV and pneumococci enhances pneumococcal virulence. Methods: We used confocal microscopy and western blot to identify the receptors involved in direct binding of RSV and pneumococci, the effects of which were studied in both in vivo and in vitro models of infection. Human ciliated respiratory epithelial cell cultures were infected with RSV for 72h and then challenged with pneumococci. Pneumococci were collected after 2h exposure and changes in gene expression determined using qRT-PCR. Results: Following incubation with RSV or purified G protein, pneumococci demonstrated a significant increase in the inflammatory response and bacterial adherence to human ciliated epithelial cultures and markedly increased virulence in a pneumonia model in mice. This was associated with extensive changes in the pneumococcal transcriptome and significant upregulation in the expression of key pneumococcal virulence genes, including the gene for the pneumococcal toxin, pneumolysin. We show that mechanistically this is due to RSV G glycoprotein binding penicillin binding protein 1a. Conclusion: The direct interaction between a respiratory virus protein and the pneumococcus resulting in increased bacterial virulence and worsening disease outcome is a new paradigm in respiratory infection. Comparison of the Streptococcus pneumoniae D39 Protein P treated compared to Protein GTreated in BEBM medium One condition design comparision of two strains including a dye swap
2014-06-21 | E-GEOD-58424 | biostudies-arrayexpress
Project description:RNASeq of the human epithelial cell line LoVo following Listeria monocytogenes infection
2015-09-15 | E-MTAB-3649 | biostudies-arrayexpress
Project description:Rapid adaptation to grow within the physiological conditions found in the host environment is an essential but poorly understood virulence requirement for systemic pathogens such as Streptococcus pneumoniae. We have now demonstrated an essential role for the one-carbon metabolism pathway and a conditional role depending on strain background for proline biosynthesis for S. pneumoniae growth in serum or CSF and therefore for systemic virulence. RNAseq data demonstrated that loss of one carbon metabolism or proline biosynthesis both have profound but differing effects on S. pneumoniae metabolism in human serum, identifying the metabolic processes dependent on each pathway during systemic infection. These data provide a more detailed understanding of the adaptations required by systemic bacterial pathogens in order to cause infection, and demonstrate that the requirement for some of these adaptations vary between strains from the same species and could therefore underpin strain variations in virulence potential.
2023-09-10 | E-MTAB-13289 | biostudies-arrayexpress