Urinary tract colonization is enhanced by a plasmid that regulates uropathogenic Acinetobacter baumannii chromosomal genes

Gisela Di Venanzio, Ana L. Flores-Mireles, Juan J. Calix, M. Florencia Haurat, Nichollas E. Scott, Lauren D. Palmer, Robert F. Potter, Michael E. Hibbing, Laura Friedman, Bin Wang, Gautam Dantas, Eric P. Skaar, Scott J. Hultgren and Mario F. Feldman ()
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Gisela Di Venanzio: Washington University School of Medicine
Ana L. Flores-Mireles: Washington University School of Medicine
Juan J. Calix: Washington University School of Medicine
M. Florencia Haurat: Washington University School of Medicine
Nichollas E. Scott: University of Melbourne at the Peter Doherty
Lauren D. Palmer: Vanderbilt University Medical Center
Robert F. Potter: Washington University School of Medicine in St. Louis
Michael E. Hibbing: Washington University School of Medicine
Laura Friedman: Universidad de Buenos Aires, Facultad de Farmacia y Bioquímica, Departamento de Microbiología, Inmunología, Biotecnología y Genética, Cátedra de Microbiología
Bin Wang: Washington University School of Medicine in St. Louis
Gautam Dantas: Washington University School of Medicine
Eric P. Skaar: Vanderbilt University Medical Center
Scott J. Hultgren: Washington University School of Medicine
Mario F. Feldman: Washington University School of Medicine

Nature Communications, 2019, vol. 10, issue 1, 1-13

Abstract: Abstract Multidrug resistant (MDR) Acinetobacter baumannii poses a growing threat to global health. Research on Acinetobacter pathogenesis has primarily focused on pneumonia and bloodstream infections, even though one in five A. baumannii strains are isolated from urinary sites. In this study, we highlight the role of A. baumannii as a uropathogen. We develop the first A. baumannii catheter-associated urinary tract infection (CAUTI) murine model using UPAB1, a recent MDR urinary isolate. UPAB1 carries the plasmid pAB5, a member of the family of large conjugative plasmids that represses the type VI secretion system (T6SS) in multiple Acinetobacter strains. pAB5 confers niche specificity, as its carriage improves UPAB1 survival in a CAUTI model and decreases virulence in a pneumonia model. Comparative proteomic and transcriptomic analyses show that pAB5 regulates the expression of multiple chromosomally-encoded virulence factors besides T6SS. Our results demonstrate that plasmids can impact bacterial infections by controlling the expression of chromosomal genes.

Date: 2019
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DOI: 10.1038/s41467-019-10706-y

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