Nosocomial endodontic Microbiome and bacteraemia
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB66454 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12121800_1.fastq.gz | Fastqsanger.gz | |||
| ERR12121800_2.fastq.gz | Fastqsanger.gz | |||
| ERR12121900_1.fastq.gz | Fastqsanger.gz | |||
| ERR12121900_2.fastq.gz | Fastqsanger.gz | |||
| ERR12121801_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 502 |
Similar Datasets
Project description:Methicillin-resistant Staphylococcus aureus (MRSA) is one of the most common causes of hospital-acquired pneumonia. To better manage patients with MRSA pneumonia, we require a greater understanding of the host-pathogen interactions during infection. MRSA research focuses on highly virulent and cytotoxic strains, which demonstrate robust phenotypes in animal models of infection. However, nosocomial infections are often caused by hospital-acquired MRSA (HA-MRSA) isolates that exhibit low cytotoxicity and few or no phenotypes in mice, thereby confounding mechanistic studies of pathogenesis. Consequently, virulence pathways utilized by HA-MRSA in nosocomial pneumonia are largely unknown. Here, we report that conditioning mice with broad-spectrum antibiotics lowers the barrier to pneumonia, thereby transforming otherwise avirulent HA-MRSA isolates into lethal pathogens. HA-MRSA isolates are avirulent in gnotobiotic mice, mimicking results in conventional animals. Thus, the observed enhanced susceptibility to infection in antibiotic-treated mice is not due to depletion of the microbiota. More generally, we found that antibiotic conditioning leads to increased susceptibility to infection by diverse antimicrobial-resistant (AMR) pathogens of low virulence. Treatment with antibiotics leads to dehydration and malnutrition, suggesting a potential role for these clinically relevant and reducible hospital complications in susceptibility to pathogens. In sum, the model described here mitigates the impact of low virulence in immunocompetent mice, providing a convenient model to gain fundamental insight into the pathogenesis of nosocomial pathogens. IMPORTANCE Antimicrobial-resistant (AMR) pathogens are responsible for over 2.8 million infections and over 35,000 deaths per year in the United States. To study these microbes, animal models that are susceptible to these pathogens are required. However, many of these pathogens exhibit low virulence in conventional mice, which has negatively impacted mechanistic studies. Here, we show that mice treated with antibiotics in their drinking water become exquisitely susceptible to low-virulence AMR pathogens. Surprisingly, the increased susceptibility was independent of the impact of antibiotics on the microbiome and seems to be due to an unintended consequence of antibiotic treatment: weight loss due to dehydration and caloric restriction. Unlike other models used to sensitize mice to low-virulence pathogens, our model does not reduce phagocyte numbers. Thus, here, we describe an immunocompetent mouse model to facilitate the identification of novel targets and accelerate the development of preventives and therapeutics to combat infections by AMR pathogens.
| S-EPMC9239109 | biostudies-literature
Project description:By using FACS-sorted MC1-ZE7 ES cells, we analyzed the genome-wide distribution of H3K27ac and DNA methylation in Zscan4 positive ES cells (Em+) and Zscan4 negative ES cells (Em-). H3K27 hyperacetylation and DNA demethylation were detected in heterochromatic regions of Em+ cells, but not Em- cells. These results suggested that the Zscan4 state takes "open" chromatin conformation in ES cells. H3K27ac in Zscan4 positive and negative cells
2015-09-10 | E-GEOD-51679 | biostudies-arrayexpress
Project description:What methylation changes are occurring in different compartments of early maturation stage seed largely remains unknown. To uncover the possible role of DNA methylation in different compartments of early maturation stage seed, we characterized the methylome of two major compartments in embryonic cotyledon: cotyledon abaxial parenchyma (EM-COT-ABPY) and cotyledon adaxial parenchyma (EM-COT-ADPY) using Illumina sequencing. Illumina sequencing of bisulfite-converted genomic DNA from cotyledon abaxial parenchyma (EM-COT-ABPY) and cotyledon adaxial parenchyma (EM-COT-ADPY) compartments.
2012-05-11 | E-GEOD-37893 | biostudies-arrayexpress
Project description:IntroductionAccording to the Centers for Disease Control's 2015 Hospital Acquired Infection Hospital Prevalence Survey, 1 in 31 hospital patients was infected with at least one nosocomial pathogen while being treated for unrelated issues. Many studies associate antibiotic administration with nosocomial infection occurrence. However, to our knowledge, there is little to no direct evidence of antibiotic administration selecting for nosocomial opportunistic pathogens.AimThis study aims to confirm gut microbiota shifts in an animal model of antibiotic treatment to determine whether antibiotic use favors pathogenic bacteria.MethodologyWe utilized next-generation sequencing and in-house metagenomic assembly and taxonomic assignment pipelines on the fecal microbiota of a urinary tract infection mouse model with and without antibiotic treatment.ResultsAntibiotic therapy decreased the number of detectable species of bacteria by at least 20-fold. Furthermore, the gut microbiota of antibiotic treated mice had a significant increase of opportunistic pathogens that have been implicated in nosocomial infections, like Acinetobacter calcoaceticus/baumannii complex, Chlamydia abortus, Bacteroides fragilis, and Bacteroides thetaiotaomicron. Moreover, antibiotic treatment selected for antibiotic resistant gene enriched subpopulations for many of these opportunistic pathogens.ConclusionsOral antibiotic therapy may select for common opportunistic pathogens responsible for nosocomial infections. In this study opportunistic pathogens present after antibiotic therapy harbored more antibiotic resistant genes than populations of opportunistic pathogens before treatment. Our results demonstrate the effects of antibiotic therapy on induced dysbiosis and expansion of opportunistic pathogen populations and antibiotic resistant subpopulations of those pathogens. Follow-up studies with larger samples sizes and potentially controlled clinical investigations should be performed to confirm our findings.
| S-EPMC7885457 | biostudies-literature
Project description:We analyzed the genome-wide chromatin states in Zscan4 positive ES cells (Em+) and Zscan4 negative ES cells (Em-) by using FACS-sorted MC1-ZE7 ES cells. H3K27 hyperacetylation and DNA demethylation were detected in heterochromatic regions of Em+ cells. These results suggested that the heterochromatin is activated in Zscan4 positive state. H3K9me2 in Zscan4 positive and negative cells
2015-09-10 | E-GEOD-58617 | biostudies-arrayexpress
Project description:By using FACS-sorted MC1-ZE7 ES cells, we analyzed the genome-wide distribution of H3K27ac and DNA methylation in Zscan4 positive ES cells (Em+) and Zscan4 negative ES cells (Em-). H3K27 hyperacetylation and DNA demethylation were detected in heterochromatic regions of Em+ cells, but not Em- cells. These results suggested that the Zscan4 state takes "open" chromatin conformation in ES cells.
2015-09-10 | GSE51679 | GEO
Project description:Extramedullary relapse (EM) of multiple myeloma (MM) is defined as infiltration of plasma cells (PC) outside of the bone marrow. EM is an aggressive form of the disease with a dismal outcome. We present cytogenetic findings of a 52-year-old female patient who was diagnosed with MM in 2008 and progression of MM to EM and plasmocellular leukemia retrospective analysis of TP53 mutation status showed presence of 2 known missense mutations in exon 6 (c.632C>T) and exon 7 (c.700T>C). EM relapse of this patient was connected to a change of the entire genome profile. We suppose that the extramedullary lesion originated by an expansion of one clone of tumor plasma cells from the bone marrow, which was confirmed by identical genomic profile of both tested samples. Thus, change of ploidy status should be considered as potential hallmark of adverse course of the disease.
2015-10-06 | E-MTAB-3600 | biostudies-arrayexpress
Project description:Non-coding sense and antisense germline transcription within the immunoglobulin heavy chain locus precedes V(D)J recombination and has been proposed to be associated with Igh locus accessibility, although its precise role remains elusive. However, no global analysis of germline transcription throughout the Igh locus has been done. Therefore, we performed directional RNAseq, demonstrating the locations and extent of both sense and antisense transcription throughout the Igh locus. Surprisingly, the majority of antisense transcripts are localized around two PAIR elements in the distal IghV region. Importantly, long-distance loops measured by 3C are observed between these two active PAIR promoters and EM-NM-<, the start site of IM-NM-< germline transcription, in a lineage- and stage-specific manner, even though this antisense transcription is EM-NM-<-independent. YY1-/- pro-B cells are greatly impaired in distal VH gene rearrangement and Igh locus compaction, and we demonstrate that YY1 deficiency greatly reduces antisense transcription and PAIR-EM-NM-< interactions. ChIP-seq shows high level YY1 binding only at EM-NM-<, but low levels near some antisense promoters. PAIR-EM-NM-< interactions are not disrupted by DRB, which blocks transcription elongation without disrupting transcription factories once they are established, but the looping is reduced after heat shock treatment, which disrupts transcription factories. We propose that transcription-mediated interactions, most likely at transcription factories, initially compact the Igh locus, bringing distal VH genes close to the DJH rearrangement, which is adjacent to EM-NM-<. Therefore, we hypothesize that one key role of non-coding germline transcription is to facilitate locus compaction, allowing distal VH genes to undergo efficient rearrangement. ChIP Seq YY1 vs. input control
2012-10-18 | E-GEOD-40822 | biostudies-arrayexpress
Project description:We analyzed the genome-wide chromatin states in Zscan4 positive ES cells (Em+) and Zscan4 negative ES cells (Em-) by using FACS-sorted MC1-ZE7 ES cells. H3K27 hyperacetylation and DNA demethylation were detected in heterochromatic regions of Em+ cells. These results suggested that the heterochromatin is activated in Zscan4 positive state.
2015-09-10 | GSE58617 | GEO
Project description:Background: Extramedullary disease (EM) in multiple myeloma (MM) is defined by escape of malignant plasma cells out of the bone marrow. The mechanisms of extramedullary spread are not well understood. MicroRNAs (miRNA) were proven to be involved in the pathogenesis of MM; nevertheless, there is a lack of knowledge about their role in EM. Methods: Using NGS analysis, we identified ten differentially expressed miRNA in plasma cells of MM versus EM patients. We performed qPCR in validation phase, using TaqMan Advanced MiRNA Assays. Results: In this study, we identified 10 miRNAs differentially expressed between MM and EM patiens.
2022-12-14 | GSE129918 | GEO