Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1145176 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30158471_1.fastq.gz | Fastqsanger.gz | |||
| SRR30158471_2.fastq.gz | Fastqsanger.gz | |||
| SRR30158472_1.fastq.gz | Fastqsanger.gz | |||
| SRR30158472_2.fastq.gz | Fastqsanger.gz | |||
| SRR30158473_1.fastq.gz | Fastqsanger.gz |
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Project description:We apply RNAseq of lung tissues to study the innate immune response to pulmonary Acinetobacter baumannii infection.
2020-05-12 | GSE143597 | GEO
Project description:Using Nanopore sequencing, our study has revealed a close correlation between genomic methylation levels and antibiotic resistance rates in Acinetobacter Baumannii. Specifically, the combined genome-wide DNA methylome and transcriptome analysis revealed the first epigenetic-based antibiotic-resistance mechanism in A. baumannii. Our findings suggest that the precise location of methylation sites along the chromosome could provide new diagnostic markers and drug targets to improve the management of multidrug-resistant A. baumannii infections.
2023-09-01 | E-MTAB-13272 | biostudies-arrayexpress
Project description:In the present work we compare the gene expression profile of A. baumannii and a mutant knock-out strain of A. baumannii lacking a small RNA gene 13573 and the corresponding small RNA 13573 over-producing strain. The main objective is to recognize the main pathways in which the small RNA 13573 is involved. Moreover, the same wild type strain was used to infect mice and was further analyzed after the infection with the aim of finding genes differentially expressed in vivo. Three biological replicates have been performed for each comparison. The RNA collection from Acinetobacter baumannii strain over-expresing the small RNA (sample 13573) was compared with this isolated from A. baumannii harboring the empty vector (PETRA sample) while gene expression in the knock-out strain (KO sample) was compared with the wild type strain Acinetobacter baumannii ATCC 17978 (ATCC sample). The RNA from A.baumannii recovered from the infected animals (INF sample) was compared with the wild type (ATCC).
2016-08-01 | E-GEOD-60348 | biostudies-arrayexpress
Project description:Acinetobacter baumannii is an important pathogen of nosocomial infection worldwide, which can primarily cause pneumonia, bloodstream infection, and urinary tract infection. The increasing drug resistance rate of A. baumannii and the slow development of new antibacterial drugs brought great challenges for clinical treatment. Host immunity is crucial to the defense of A. baumannii infection, and understanding the mechanisms of immune response can facilitate the development of new therapeutic strategies. To obtain the system-level changes of host proteome in immune response, we used TMT labeling quantitative proteomics to compare the proteome changes of lungs from A. baumannii infected mice with control mice six hours after infection. A total of 6218 proteins were identified in which 6172 could be quantified. With threshold p < 0.05 and fold change > 1.2, we found 120 differentially expressed proteins. Bioinformatics analysis showed that differentially expressed proteins after infection were associated with receptor recognition, NADPH oxidase (NOX) activation and antimicrobial peptides. These differentially expressed proteins were involved in the pathways including leukocyte transendothelial migration, phagocyte, neutrophil degranulation, and antimicrobial peptides. In conclusion, our study showed proteome changes in mouse lung tissue due to A. baumannii infection and suggested the important roles of NOX, neutrophils, and antimicrobial peptides in host response. Our results provide a potential list of proteins candidates for the further study of host-bacteria interaction in A. baumannii infection.
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Project description:Acinetobacter baumannii is an emerging nosocomial pathogen that causes severe infections such as pneumonia or blood stream infections. As the incidence of multidrug-resistant A. baumannii infections in intensive care units increases, the pathogen is considered of greater clinical concern. Little is known about the molecular interaction of A. baumannii with its host yet. In order to study the host cell response upon A. baumannii infection, a complexome analysis was performed. For this, we identified a virulent ( A. baumannii 2778) and a non virulent (A. baumannii 1372) clinical isolate of genetic similarity > 95 % (both isolates from IC 2 harboring OXA 23). HUVECs were infected with each strain and enriched mitochondrial fraction was used for complexome profiling. Complexome analysis identified dramatic reduction of mitochondrial protein complexes in the strain of greater virulence.
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Project description:Acinetobacter baumannii is a highly pathogenic and multidrug-resistant Gram-negative bacterium that causes severe nosocomial infections. To better understand the mechanism of pathogenesis, we compare the proteomes of uninfected and infected human cells, revealing that transcription factor FOS is the host protein most strongly induced by A. baumannii infection. Pharmacological inhibition of FOS reduces the cytotoxicity of A. baumannii in cell-based models, and similar results are also observed in a mouse infection model. A. baumannii outer membrane vesicles (OMVs) are shown to activate the aryl hydrocarbon receptor (AHR) of host cells by inducing the host enzyme tryptophan-2,3-dioxygenase (TDO), producing the ligand kynurenine, which binds AHR. Following ligand binding, AHR is a direct transcriptional activator of the FOS gene. Our results suggest that bacterial infection interacts with host tryptophan metabolism and the transcription factor FOS.
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Project description:Two Acinetobacter baumannii strains with low susceptibility to fosmidomycin and two reference with high susceptibility to fosmidomycin were DNA-sequenced to investigate the genomic determinants of fosmidomycin resistance.
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Project description:Analysis of the effect of human pleural fluid on the transcriptome of Acinetobacter baumanii A118 Acinetobacter baumannii (Ab) is one of the most treacherous pathogens among those causing hospital-acquired pneumonia (HAP). A. baumannii possesses an adaptable physiology, seen not only in its antibiotic resistance and virulence phenotypes, but also in its metabolic versatility. In this study, we observed that A. baumannii undergoes global transcriptional changes in response to human pleural fluid (PF), a key host-derived environmental signal. Differential gene expression analyses combined with experimental approaches revealed changes in A. baumannii metabolism, affecting cytotoxicity, persistence, bacterial killing and chemotaxis. Over 55% of the differentially expressed transcriptomic genes corresponded to metabolic processes, including the up regulation of glutamate, short chain fatty acid, and styrene metabolism. We observed an up regulation of the pyruvate dehydrogenase complex and found that pyruvate (PYR), in conjunction with PF, triggers an A. baumannii pathogenic behavior that adversely impacts human epithelial cell viability. Interestingly, PF also amplified A. baumannii cytotoxicity against murine macrophages, suggesting an immune evasion strategy implemented by A. baumannii. Moreover, we uncovered opposing metabolic strategies dependent on the degree of pathogenicity of the strains, where less pathogenic strains demonstrated greater utilization of PYR to promote persister formation in the presence of PF. Additionally, our transcriptomic analysis and growth studies of A. baumannii suggest the existence of an alternative phenylalanine (PA) catabolic route independent of the phenylacetic acid pathway, which converts PA to phenylpyruvate (PP) and shuttles intermediates into styrene metabolism. This alternative route promoted a neutrophil-evasive state, as PF-induced degradation of PP significantly reduced overall human neutrophil chemotaxis in ex vivo chemotactic assays. Taken together, these data highlights A. baumannii pathoadaptabililty in response to host signals and provide further insight into the role of bacterial metabolism in virulence traits, antibiotic persistence strategies, and host innate immune evasion.
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Project description:Acinetobacter baumannii causes high mortality in ventilator-associated pneumonia patients and antibiotic treatment is compromised in multi-drug resistant strains resistant to beta-lactams, carbapenems, cephalosporins, polymyxins and tetracyclines. Among COVID-19 patients receiving ventilator support, multi-drug resistant A. baumannii secondary infection is associated with a two-fold increase in mortality. Here we investigated the use of the 8-hydroxyquinoline ionophore PBT2 to break resistance of A. baumannii to tetracycline class antibiotics.
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Project description:Acinetobacter baumannii A1S_1874 gene encodes as a LysR-type transcriptional regulator. LysR family regulators known to regulate biofilm formation, antibiotic resistance, and the expression of diverse genes in other Gram-negative bacteria. However, A1S-1874 has never been characterized in Acinetobacter baumannii, and the studies about the regulon of A1S-1874 are not discovered. In this study we revealed that A1S_1874 differentially regulates at least 302 genes including the csu pilus operon, N-acylhomoserine lactone synthese gene, A1S_0112-A1S_0118 operon, type 1v secretion system related genes that are involved in biofilm formation, surface motility, adherence, quorum sensing and virulence. Overall, our data suggests that A1S-1874 is a key regulator of Acinetobacter baumannii biofilm formation and gene expression.
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