Staphylococcus epidermidis RP62A
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR9493380.fastq.gz | Fastqsanger.gz | |||
| SRR9493376.fastq.gz | Fastqsanger.gz | |||
| SRR9493377.fastq.gz | Fastqsanger.gz | |||
| SRR9493378.fastq.gz | Fastqsanger.gz |
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Project description:RNASeq identified several pathways that were differentially expressed/regulated in the small intestines that correlated with intestinal failure during toxic shock syndrome caused by staphylococcal superantigen in a humanized mouse model
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Project description:252 dengue fever patients and 159 dengue shock syndrome patients
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Project description:BACKGROUND: Infections with community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) are emerging worldwide. We investigated an outbreak of severe CA-MRSA infections in children following out-patient vaccination. METHODS AND FINDINGS: We carried out a field investigation after adverse events following immunization (AEFI) were reported. We reviewed the clinical data from all cases. S. aureus recovered from skin infections and from nasal and throat swabs were analyzed by pulse-field gel electrophoresis, multi locus sequence typing, PCR and microarray. In May 2006, nine children presented with AEFI, ranging from fatal toxic shock syndrome, necrotizing soft tissue infection, purulent abscesses, to fever with rash. All had received a vaccination injection in different health centres in one District of Ho Chi Minh City. Eight children had been vaccinated by the same health care worker (HCW). Deficiencies in vaccine quality, storage practices, or preparation and delivery were not found. Infection control practices were insufficient. CA-MRSA was cultured in four children and from nasal and throat swabs from the HCW. Strains from children and HCW were indistinguishable. All carried the Panton-Valentine leukocidine (PVL), the staphylococcal enterotoxin B gene, the gene complex for staphylococcal-cassette-chromosome mec type V, and were sequence type 59. Strain HCM3A is epidemiologically unrelated to a strain of ST59 prevalent in the USA, although they belong to the same lineage. CONCLUSIONS: We describe an outbreak of infections with CA-MRSA in children, transmitted by an asymptomatic colonized HCW during immunization injection. Consistent adherence to injection practice guidelines is needed to prevent CA-MRSA transmission in both in- and outpatient settings. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-45
2009-01-16 | E-BUGS-45 | biostudies-arrayexpress
Project description:Around 700,000 SNPs were genotyped in 290 controls, 252 dengue fever patients and 159 dengue shock syndrome patients from Thailand.
| EGAS00001002756 | EGA
Project description:ABSTRACT Background. Acute Kawasaki disease (KD) is difficult to distinguish from other acute rash/fever illnesses, in part because the etiologic agent(s) and pathophysiology remain poorly characterized. As a result, diagnosis and critical therapies may be delayed. Methods. We used DNA microarrays to identify possible diagnostic features of KD. We compared gene expression patterns in the blood of 23 children with acute KD and 18 age-matched febrile children with three illnesses that resemble KD. Results. Genes associated with platelet and neutrophil activation were expressed at higher levels in KD patients than in patients with acute adenovirus infections or systemic adverse drug reactions but not in patients with scarlet fever; genes associated with B cell activation were also expressed at higher levels in KD patients than in controls. A striking absence of interferon-stimulated gene expression in the KD patients was confirmed in an independent cohort of KD subjects. We successfully predicted the diagnosis in 21 of 23 KD patients and 7 of 8 adenovirus patients using a set of 38 gene transcripts. Conclusions. These findings provide insight into the molecular features that distinguish KD from other febrile illnesses, and support the feasibility of developing novel diagnostic reagents for KD based on the host response. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Disease State: One of Kawasaki Disease (KD) or control (C) of Scarlet fever (C-sf), adenovirus infection (C-ai) or drug reaction (C-dr) disease_state_design
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Project description:Streptococcus pyogenes (Group A Streptococcus: GAS) is a major human pathogen that causes streptococcal pharyngitis, skin and soft-tissue infections, and life-threatening conditions such as streptococcal toxic shock syndrome (STSS). A large number of virulence-related genes are encoded on GAS genomes, which are involved in host-pathogen interaction, colonization, immune invasion, and long-term survival within hosts, causing the diverse symptoms. Here, we investigated the interaction between GAS-derived extracellular vesicles and host cells in order to reveal pathogenicity mechanisms induced by GAS infection.
2021-05-17 | PXD026040 | JPOST Repository
Project description:Staphylococcus aureus, a gram-positive bacterium, causes food poisoning and toxic shock syndrome through the production of superantigenic toxins known as Staphylococcal enterotoxins serotypes A-J (SEA, SEB, etc.) and toxic shock syndrome toxin-1 (TSST-1). A subset of these toxins have been classified as potential biothreat agents. The chronology of molecular events that could potentially characterize superantigenic toxicity and early pathogenesis is not well understood. The focus of this study was to determine the distinct and shared mechanisms of response to three toxins of the superantigenic family, namely SEA, SEB and TSST-1. Since skin functions as the front line of the host’s defense mechanism, melanocytes were selected for the study and treated with 25 µg/mL of one of these three toxins. Cells were collected after treatment for six different time periods, ranging from 0.5 h to 48 h. Total RNA was investigated using gene expression microarrays containing approximately 50,000 probes, and a subset of the results were validated using NanoString assays. Transcriptomic expression data indicated that each of these three toxins had a unique longitudinal trajectory. In particular, the gene expression profiles of SEB post-exposure was very distinct from those for SEA and TSST-1 superantigens. All three superantigens showed enriched biological networks related to necrosis, skin disorders, and inflammation. The three superantigens share some similarities in acting on the mechanisms underlying apoptosis, innate immunity, and other biological processes. Pathways related to innate immunity, such as the patterns of cytokine production and acute-phase response, showed toxin-specific regulation. The differentially regulated networks can be logical targets for early therapeutic intervention and can potentially serve as early diagnostic markers for superantigen-induced toxicity.
2022-06-30 | GSE124756 | GEO
Project description:Infection with dengue viruses (DENVs) leads to a spectrum of disease outcomes. The pathophysiology of severe versus non-severe manifestations of DENV infection may be driven by host responses, which could be reflected in the transcriptional profiles of peripheral blood immune cells. We conducted genome-wide microarray analysis of whole blood RNA from 34 DENV-infected children in Nicaragua collected on days 3–6 of illness, with different disease manifestations. Gene expression analysis identified genes that are differentially regulated between clinical subgroups. The most striking transcriptional differences were observed between dengue patients with and without shock, especially in the expression of mitochondrial ribosomal proteins associated with protein biosynthesis. In the dengue hemorrhagic fever patients, one subset of differentially expressed genes encode neutrophil-derived anti-microbial peptides associated with innate immunity. We analyzed 44 HEEBO arrays on which were hybridized RNA amplified from whole blood collected into PAXgene tubes. 34 samples were collected from DENV-infected patients who presented between days 3-6 of illness. Six convalescent samples collected 14-19 days after onset of symptoms were from two dengue fever patients, one dengue hemorrhagic fever patient and three dengue shock syndrome patients. Additionally, samples from four normal healthy individuals were also analyzed.
2010-11-20 | E-GEOD-25226 | biostudies-arrayexpress
Project description:The molecular basis of interindividual clinical variability upon infection with Staphylococcus aureus is unclear. We describe patients with haploinsufficiency for the linear deubiquitinase OTULIN, encoded on chromosome 5p. The patients suffer from episodes of life-threatening necrosis, typically triggered by S. aureus infections. The disorder is phenocopied in patients with the 5p- (Cri-du-Chat) chromosomal deletion syndrome. OTULIN haploinsufficiency causes an accumulation of linear ubiquitin in dermal fibroblasts, but TNF-receptor NF-κB-signaling remains intact. Blood leukocyte subsets are unaffected. The OTULIN-dependent accumulation of caveolin-1 in dermal fibroblasts — but not leukocytes — facilitates the cytotoxic damage inflicted by the staphylococcal virulence factor α-toxin. Naturally elicited antibodies to α-toxin contribute to incomplete clinical penetrance. By disrupting cell-intrinsic immunity to α-toxin in non-leukocytic cells, human OTULIN haploinsufficiency underlies life-threatening staphylococcal disease.
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Project description:Background Deciphering host responses contributing to dengue shock syndrome (DSS), the life-threatening form of acute viral dengue infections, is required to improve both the differential prognosis and the treatments provided to DSS patients, a challenge for clinicians. Methodology/Principal Findings Based on a prospective study, we analyzed the genome-wide expression profiles of whole blood cells from 48 matched Cambodian children: 19 progressed to DSS while 16 and 13 presented respectively classical dengue fever (DF) or dengue hemorrhagic fever grades I/II (DHF). Using multi-way analysis of variance (ANOVA) and adjustment of p-values to control the False Discovery Rate (FDR<10%), we identified a signature of 2959 genes differentiating DSS patients from both DF and DHF, and showed a strong association of this DSS-gene signature with the dengue disease phenotype. Using a combined approach to analyse the molecular patterns associated with the DSS-gene signature, we provide an integrative overview of the transcriptional responses altered in DSS children. In particular, we show that the transcriptome of DSS children blood cells is characterized by a decreased abundance of transcripts related to T and NK lymphocyte responses and by an increased abundance of anti-inflammatory and repair/remodeling transcripts. We also show that unexpected pro-inflammatory gene patterns at the interface between innate immunity, inflammation and host lipid metabolism, known to play pathogenic roles in acute and chronic inflammatory diseases associated with systemic vascular dysfunction, are transcriptionnally active in the blood cells of DSS children. Conclusions/Significance We provide a global while non exhaustive overview of the molecular mechanisms altered in of DSS children and suggest how they may interact to lead to final vascular homeostasis breakdown. We suggest that some mechanisms identified should be considered putative therapeutic targets or biomarkers of progression to DSS. Whole blood genome-wide expression profiles of Cambodian children (3-15 year old) infected with dengue virus, having different clinical outcomes were compared. The studied cohort included 16 acute dengue fever samples, 13 acute dengue hemorrhagic fever samples and 19 acute dengue shock syndrome samples, classified according to the 1997 WHO criteria and randomised for age, gender, viral serotype and day of blood sampling after onset of fever. Microarray data were normalised using the quantile method. Multi-way ANOVA was used to compared the three clinical groups, at several False Discovery Rate of 10. Unsupervised Hierarchical Clustering (TreeView) showed that DSS patients clustered together (17 out of 19), identifying a gene-signature of DSS. Bio-informatics-based analysis using the demonstration version 7.1 of Ingenuity Pathway Analysis software (IPA; Ingenuity Systems, www.ingenuity.com) associated with manual and litterature-based analysis was carried out to identify the most relevant functional processes associated with the identified DSS gene expression profile. This was done by combining most informative canonical pathways identified using IPA, genes having the strongest association with the disease phenotype based on ANOVA analysis, and similarities to molecular patterns altered in other systemic inflammatory processes associated with endothelial dysfunction.
2010-07-21 | E-GEOD-17924 | biostudies-arrayexpress