Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1198891 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We performed RNAseq for gene expression analysis for six strains of Acinetobacter Baumannii isolated from blood samples (defined as strains 1, 2, 3, 4 and 6) of patients hospitalized at the University Hospital \\"San Giovanni di Dio e Ruggi d'Aragona\\" (Salerno, Italy)
2023-09-01 | E-MTAB-13274 | biostudies-arrayexpress
Project description:Acinetobacter baumannii is a pathogen, highly adaptable to both hospital and host-associated environments. Understanding the genetic mechanisms underlying its adaptability is critical for controlling its persistence. Our study identified the crp-osmC gene cluster, flanked by ISAba1 elements, as a significant genetic structure undergoing amplification in A. baumannii. By experimentally mimicking the amplification of this gene cluster, we found that it substantially enhanced bacterial growth and competitiveness, while also increasing biofilm formation and serum resistance. Furthermore, amplification of the crp-osmC cluster enhanced colonization in murine infection models. Notably, this amplification was largely limited to the epidemic ST2 lineage clinical isolates. Intriguingly, gene amplification was also accompanied by heightened susceptibility to several antibiotics. Overall, ISAba1-mediated amplification of the crp-osmC cluster enhances host-associated fitness in A. baumannii, while the accompanying increase in antibiotic sensitivity reflects a trade-off between survival and resistance.
2026-05-20 | GSE331122 | GEO
Project description:Purpose: The goal of this study was to elucidate the collateral effects associated with OXA-23 overexpression on the Acinetobacter baumannii global transcriptome. Results: Besides the 99.73-fold increase in blaOXA-23 transcript upon IPTG induction, no other transcripts showed more than a 2-fold change compared to the wildtype control. This suggests that OXA-23 over expression to levels similarly observed in multi drug resistant A. baumannii clinical isolates does not effect the transcriptome.
2021-11-15 | GSE185203 | GEO
Project description:In recent years, the Gram-negative bacterium Acinetobacter baumannii has garnered considerable attention for its unprecedented capacity to rapidly develop resistance to antibacterial therapeutics. This is coupled with the seemingly epidemic emergence of new hyper-virulent strains. Although strain-specific differences for A. baumannii isolates have been well described, these studies have primarily focused on proteinaceous factors. At present, only limited publications have investigated the presence and role of small regulatory RNA (sRNA) transcripts. Herein, we perform such an analysis, describing the RNA-seq-based identification of 78 A. baumannii sRNAs in the AB5075 background. Together with six previously identified elements, we include each of these in a new genome annotation file, which will serve as a tool to investigate regulatory events in this organism. Our work reveals that the sRNAs display high expression, accounting for >50 % of the 20 most strongly expressed genes. Through conservation analysis we identified six classes of similar sRNAs, with one found to be particularly abundant and homologous to regulatory, C4 antisense RNAs found in bacteriophages. These elements appear to be processed from larger transcripts in an analogous manner to the phage C4 molecule and are putatively controlled by two further sRNAs that are strongly antisense to them. Collectively, this study offers a detailed view of the sRNA content of A. baumannii, exposing sequence and structural conservation amongst these elements, and provides novel insight into the potential evolution, and role, of these understudied regulatory molecules. This study is based on the annotation of novel sRNAs on basis of an Acinetobacter baumannii RNA sequencing dataset. Each sample was generated by pooling three independent biological replicate RNA preps
2016-03-30 | E-GEOD-75708 | biostudies-arrayexpress
Project description:Acinetobacter baumannii is associated with severe hospital-acquired multi-drug resistant infections worldwide, causing significant mortality and morbidity in intensive care patients or under prolonged hospitalization. Multiple studies have recently shown that a proportion of circulating clinical isolates establish a transient multiplication niche inside phagocytic and non-phagocytic eukaryotic cells. We have previously demonstrated that the A. baumannii ABC141 strain invades human endothelial and epithelial cells, where it efficiently multiplies without induction of cytotoxicity. Here, we show that ABC141 adhesion, invasion, and intracellular multiplication depend on the growth stage, being most efficient in the exponential growth phase. To define the gene expression signature most favorable to an intracellular lifestyle, a transcriptomic comparison was carried out between exponentially grown ABC141 and cultures at the stationary phase. Although most of the pathways identified reflected growth-related metabolic changes, we observed an upregulation of the twin-arginine translocation (Tat) export system. Analysis of a mutant strain lacking the tatABC operon revealed this secretion system is only required for adhesion to host cells but not invasion and intracellular multiplication. These data highlight a new role for the Tat export pathway in A. baumannii pathogenesis.
2025-08-12 | GSE295948 | GEO
Project description:Acinetobacter baumannii is often highly resistant to multiple antimicrobials, posing a risk of treatment failure, and colistin is a "last resort" for treatment of the bacterial infection. However, colistin resistance is easily developed when the bacteria are exposed to the drug, and a comprehensive analysis of colistin-mediated changes in colistin-susceptible and -resistant A. baumannii is needed. In this study, using an isogenic pair of colistin-susceptible and -resistant A. baumannii isolates, alterations in morphologic and transcriptomic characteristics associated with colistin resistance were revealed. Whole-genome sequencing showed that the resistant isolate harbored a PmrBL208F mutation conferring colistin resistance, and all other single-nucleotide alterations were located in intergenic regions. Using scanning electron microscopy, it was determined that the colistin-resistant mutant had a shorter cell length than the parental isolate, and filamented cells were found when both isolates were exposed to the inhibitory concentration of colistin. When the isolates were treated with inhibitory concentrations of colistin, more than 80% of the genes were upregulated, including genes associated with antioxidative stress response pathways. The results elucidate the morphological difference between the colistin-susceptible and -resistant isolates and different colistin-mediated responses in A. baumannii isolates depending on their susceptibility to this drug.
2025-05-02 | GSE267612 | GEO