PhD, Michigan State University
BS, Pennsylvania State University
Assistant Professor, Department of Microbiology and Molecular Genetics
Member, Molecular Virology and Microbiology Graduate Program
Bomberger Lab Overview:
The Bomberger lab studies host-pathogen interactions, and more specifically, how each influences the other during an infection. Emerging evidence reveals that pathogens have the ability to modulate the host response to infection, while at the same time, respond to host defense by altering their virulence and antibiotic resistance. We examine the interaction between the opportunistic pathogen, Pseudomonas aeruginosa, respiratory viruses (like influenza, rhinovirus and respiratory syncytial virus) and the host airway epithelium as a model system to investigate the broader question of how the host impacts a pathogen in the context of an infection, and vice versa.
Most co-infection studies to date characterize an infection where the virus predisposes patients for a secondary bacterial infection, but scientists and clinicians now recognize that the synergism is not unidirectional (Tashiro et al. 1987). Hussell et al. suggested that simultaneous infections are the norm, not the exception, and that co-infection with multiple pathogens may alter the immune response compared to either pathogen alone (Hussell and Williams 2004). Surprisingly, given the abundance of literature documenting influenza and bacterial dual infections, including those infections involving P. aeruginosa, the mechanisms responsible for this viral-bacterial synergy in the lung remains poorly understood. Using live-cell imaging, cell biological, microbiological and immunological assays, we explore mechanisms by which respiratory pathogens synergize in the host to promote each other’s colonization.
- Examining the mechanism by which the host’s innate immune response to a respiratory viral infection promotes P. aeruginosa bacterial biofilm growth and the development of antibiotic resistance.
- Characterizing the cell biological mechanism, in P. aeruginosa, that allows differential virulence factor secretion in response to host cytokines.
Jordan Gaston, Research Technician
Abiola Ogunsola, Research Technician
Becca Flitter, Postdoctoral Fellow
Jeffrey Melvin, Postdoctoral Fellow
Megan Kiedrowski, Postdoctoral Fellow
Matthew Hendricks, Graduate Student
Anna Zemke, Assistant Professor (Department of Pulmonary and Critical Care Medicine)
Areas of Interest
host-pathogen interactions; respiratory infections; viral-bacterial co-infections; epithelial cell biology; protein trafficking and biochemistry; Cystic Fibrosis; COPD
Bomberger J. M, Coutermarsh B. A, Barnaby R. L, and Stanton B. A. Arsenic promotes ubiquitinylation and lysosomal degradation of cystic fibrosis transmembrane conductance regulator (CFTR) chloride channels in human airway epithelial cells. J Biol Chem. 287: 17130-17139. | View Abstract
Bomberger J. M, Ye S, Maceachran D. P, Koeppen K, Barnaby R. L, O'Toole G. A, and Stanton B. A. A Pseudomonas aeruginosa toxin that hijacks the host ubiquitin proteolytic system. PLoS Pathog. 7: e1001325. | View Abstract
Bahl C. D, Morisseau C, Bomberger, J. M, Stanton B. A, Hammock B. D, O'Toole G. A, and Madden D. R. Crystal structure of the cystic fibrosis transmembrane conductance regulator inhibitory factor Cif reveals novel active-site features of an epoxide hydrolase virulence factor. J Bacteriol. 192: 1785-1795. | View Abstract
Bomberger J. M, Maceachran D. P, Coutermarsh B. A, Ye S, O'Toole G. A, and Stanton B. A. Long-distance delivery of bacterial virulence factors by Pseudomonas aeruginosa outer membrane vesicles. PLoS Pathog. 5: e1000382. | View Abstract
Bomberger J. M, Barnaby R. L, and Stanton B. A. The deubiquitinating enzyme USP10 regulates the post-endocytic sorting of cystic fibrosis transmembrane conductance regulator in airway epithelial cells. J Biol Chem. 284: 18778-18789. | View Abstract
Moreau-Marquis S, Bomberger J. M, Anderson G. G, Swiatecka-Urban A, Ye S, O'Toole G. A, and Stanton B. A. The DeltaF508-CFTR mutation results in increased biofilm formation by Pseudomonas aeruginosa by increasing iron availability. Am J Physiol Lung Cell Mol Physiol. 295: L25-37. | View Abstract
MacEachran D. P, Ye S, Bomberger J. M, Hogan D. A, Swiatecka-Urban A, Stanton B. A, O'Toole G. A. The Pseudomonas aeruginosa secreted protein PA2934 decreases apical membrane expression of the cystic fibrosis transmembrane conductance regulator. Infect Immun. 75: 3902-3912. | View Abstract