Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1125445 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR29456493.fastq.gz | Fastqsanger.gz | |||
| SRR29456494.fastq.gz | Fastqsanger.gz | |||
| SRR29456495.fastq.gz | Fastqsanger.gz | |||
| SRR29456496.fastq.gz | Fastqsanger.gz | |||
| SRR29456497.fastq.gz | Fastqsanger.gz |
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Project description:Neonatal meningitis and neurocomplications are often a complication of neonatal bacterial bloodstream infections. As distinct bacterial organisms may cause different disease outcomes, we assessed two separate bacterial infections: E. coli and S. agalactiae (GBS). In this study we assessed differences in immune response within the brain tissue of neonates and the effect of gamma delta T cells to the brain during bacterial infection. As gamma delta T cells are resident to tissues, and can contribute to bacterial infections, we compared wild-type and TCRdKO mice, which lack gamma delta T cells, in two infections models: E. coli and GBS.
2024-01-16 | GSE253301 | GEO
Project description:Diabetic wound infections have poor healing outcomes due to the presence of numerous pathogens in addition to an impaired immune response. Group B Streptococcus (GBS) is one of the most commonly isolated bacteria from diabetic wound infections, but virulence mechanisms GBS uses during these infections have not been investigated. Here, we developed a new murine model of GBS diabetic wound infection to determine how GBS establishes infection and persists in the wound environment. Using dual RNA sequencing, we demonstrate that GBS infection of diabetic wounds triggers an inflammatory response, leading to increased transcript levels of inflammatory cytokines and chemokines as well as markers of neutrophil degranulation such as myeloperoxidase, calprotectin, and elastase. We then confirm that diabetic wounds infected with GBS have significantly higher abundance of Il-1b, KC (CXCL1), myeloperoxidase, calprotectin and elastase in wound tissues than uninfected controls . When examining how GBS adapts to this hyper-inflammatory environment we find that GBS upregulates numerous virulence factors including the surface plasminogen-binding protein pbsP, the nuclease nucA, the cyl operon which is responsible for hemolysin production and pigmentation as well as numerous effectors of type VII secretion. In addition, we recovered multiple hyper-pigmented/hemolytic GBS colonies from the murine diabetic wound environment which encode mutations in the two-component system covRS. We then go on to demonstrate that a mutant in cylE, which is repressed by CovR, is attenuated in diabetic wound infection. Finally, we examine the most highly upregulated gene pbsP in diabetic wound infection and find that PbsP is necessary for diabetic wound infection via adherence to the skin and promotion of inflammation.
2022-09-30 | GSE201342 | GEO
Project description:Streptococcus agalactiae (Group B Streptococcus, GBS) can colonize the human vaginal tract leading to both superficial and serious infections in adults and neonates. To study bacterial colonization of the reproductive tract in a mammalian system, we employed a murine vaginal carriage model. Using RNASeq, the transcriptome of GBS growing in vivo during vaginal carriage was determined. Over one-quarter of the genes in GBS were found to be differentially regulated during in vivo colonization as compared to laboratory cultures. A two-component system (TCS) homologous to the staphylococcal virulence regulator SaeRS was identified as being up-regulated in vivo. One of the SaeRS targets, pbsP, a proposed GBS vaccine candidate, was shown to be important for colonization of the vaginal tract. A component of vaginal lavage fluid acted as a signal to turn on pbsP expression via SaeRS. These data demonstrate the ability to quantify RNA expression directly from the murine vaginal tract and identify novel genes involved in vaginal colonization by GBS. They also provide more information about the regulation of an important virulence and colonization factor of GBS, pbsP, by the TCS SaeRS.
2018-02-06 | GSE109680 | GEO
Project description:INSeq of Citrobacter freundii during bloodstream infection
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Project description:The aim of this study was to investigate the response of human brain endothelial cells to bacterial (group B streptococcus, GBS) infection. Results: GBS WT strain infection results in a specific gene induction pattern that is different from the pilA mutant, but not other mutants such as pilB and srr-1. Conclusion: These findings suggest that the GBS PilA protein contributes to gene induction in brain endothelium.
2011-09-06 | E-MTAB-765 | biostudies-arrayexpress
Project description:Group B Streptococcus (GBS) is a pervasive perinatal pathogen, yet factors driving GBS dissemination in utero are poorly defined. Gestational diabetes mellitus (GDM), a complication marked by dysregulated immunity and maternal microbial dysbiosis, increases risk for GBS perinatal disease. We interrogated host-pathogen dynamics in a novel murine GDM model of GBS colonization and perinatal transmission. GDM mice had greater GBS in utero dissemination and subsequently worse neonatal outcomes. Dual-RNA sequencing revealed differential GBS adaptation to the GDM reproductive tract, including a putative glycosyltransferase (yfhO), and altered host responses. GDM disruption of immunity included reduced uterine natural killer cell activation, impaired recruitment to placentae, and altered vaginal cytokines. Lastly, we observed distinct vaginal microbial taxa associated with GDM status and GBS invasive disease status. Our translational model of GBS perinatal transmission in GDM hosts recapitulates several clinical aspects and enables discovery of host and bacterial drivers of GBS perinatal disease.
2023-07-05 | GSE236335 | GEO
Project description:We have conducted RNA-seq analysis on Group B Streptococcus (GBS) when interacting with human stem-cell (hSC) derived BECs. The study contains a control group for GBS and a control group for BECs each with three biological replicates. The last group contains GBS infection BECs and also has three replicates.
2024-04-23 | GSE197489 | GEO
Project description:Early onset sepsis due to Group B streptococcus (GBS) leads to neonatal morbidity, increased mortality and long term neurological deficencies. Interaction between septicemic GBS and confluent monlayers of human coronary artery endothelial cells (HCAEC) was analyzed by a genome wide expression profiling. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real Time RT-PCR assay (Granulocyte chemotactic protein 2 (CXCL6)), ELISA (Urokinase, Cyclooxygenase 2 (COX2), Granulocyte chemotactic protein 1 (IL8)) and Western Blotting (Heme oxygenase1, BCL2 interacting protein (BIM)) at various time points between 4 and 24 hours. In total, 124 genes were differentially regulated (89 upregulated, 35 downregulated) based on a more than 3-fold difference to unstimulated HCAEC. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, infection and inflammation. We confirmed upregulation of urokinase (UPA), COX2, HMOX1 and BCL2 interacting protein and downregulation of CXCL6 and IL8. These results indicate that GBS infection might lead to impaired function of the innate immune system and might contribute to hemorrhagic and inflammatory complications during GBS sepsis. Keywords: stimulated HCAEC (with S. agalactiae) vs unstimulated control cells total samples analysed are 2, including control
2010-12-31 | E-GEOD-15495 | biostudies-arrayexpress
Project description:Group B Streptococcus (GBS) infection during pregnancy
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