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: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.