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)
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.
Project description:We report the transcriptional expression from wild type, a ponA mutant, and lipooligosaccharide-deficient A. baumannii in order to understand the cellular changes after inactivation of lipid A biosynthesis. Among all strains, genes in the Localization Of Lipoprotein (Lol) transport pathway were upregulated. This study provides a framework to understand how some Acinetobacter baumannii strains can survive without lipid A and lipopolysaccharide/lipooligosaccharide.
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.
Project description:Acinetobacter baumannii AB042, a triclosan-resistant mutant, was examined for modulated gene expression using whole genome sequencing, transcriptomics, and proteomics in order to understand the mechanism of triclosan-resistance as well as its impact on A. Baumannii.
Project description:Objectives: Colistin remains a last-line treatment for multidrug-resistant Acinetobacter baumannii and combined use of colistin and carbapenems has shown synergistic effects against multidrug-resistant strains. In order to understand the bacterial responses to these antibiotics we analysed the transcriptome of A. baumannii following exposure to each.
Project description:Acinetobacter baumannii is a Gram-negative pathogen that has emerged as one of the most troublesome pathogens for health care institutions globally. Bacterial quorum sensing (QS) is a process of cell-to-cell communication that relies on the production, secretion and detection of autoinducer (AI) signals to share information about cell density and regulate gene expression accordingly. The molecular and genetic basis of Acinetobacter baumannii virulence remains poorly understood. Therefore, the contribution of the abaI/abaR quorum sensing system to growth characteristics, morphology, biofilm formation, resistance, motility and virulence of Acinetobacter baumannii was studied in detail. RNA-seq analysis indicated that genes involved in various aspects of energy production and conversion, Valine, leucine and isoleucine degradation and lipid transport and metabolism are associated with bacterial pathogenicity. Our work provides a new insight into abaI/abaR quorum sensing system effects pathogenicity in A. baumannii. We propose that targeting the AHL synthase enzyme abaI could provide an effective strategy for attenuating virulence. On the contrary, interdicting the autoinducer synthase–receptor abaR elicits unpredictable consequences, which may lead to enhanced bacterial virulence.
2021-04-28 | GSE173396 | GEO
Project description:Transmission of extended-drug resistant Acinetobacter baumannii in a tertiary care hospital in Mexico city
