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.
Project description:Nosocomial outbreaks of infections caused by multidrug-resistant Acinetobacter baumannii have emerged as a serious threat to human health. The phosphoproteomics of pathogenic bacteria have been investigated for their role in virulence regulation networks. In this study, we analyzed the phosphoproteomics of two clinical isolates of A. baumannii: imipenem-sensitive strain SK17-S and -resistant strain SK17-R.
Project description:Asymptomatic gut colonization increases the risk of clinical infection and transmission by the multidrug-resistant pathogen Acinetobacter baumannii. Ornithine utilization was shown to be critical for A. baumannii competition with the resident microbiota to persist in gut colonization, but the regulatory mechanisms and cues are unknown. Here, we identify a transcriptional regulator, AstR, that specifically activates the expression of the A. baumannii ornithine utilization operon astNOP. Phylogenetic analysis suggests that AstR was co-opted from the Acinetobacter arginine utilization ast(G)CADBE locus and is specialized to regulate ornithine utilization in A. baumannii. Reporter assays showed that astN promoter expression was activated by ornithine but inhibited by glutamate and other preferred amino acids. astN promoter expression was similarly activated by incubation with fecal samples from conventional mice but not germ-free mice, suggesting AstR-dependent activation of the astN promoter responds to intermicrobial competition for amino acids. Finally, AstR was required for A. baumannii to colonize the gut in a mouse model. Together, these results suggest that pathogenic Acinetobacter species evolved AstR to regulate ornithine catabolism, which is required to compete with the microbiota during gut colonization.
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.
2023-04-10 | PXD035235 | Pride
Project description:Epidemiology of clinical carbapenem- resistant Acinetobacter baumannii isolates in China
