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Alan R. Hauser, MD, PhDAssistant Professor
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To visit the Hauser Lab website click here.
P. aeruginosa is a gram-negative opportunistic pathogen that causes a variety of disease manifestations in humans, including pneumonia, sepsis, and urinary tract infections. Although many putative P. aeruginosa virulence factors have been identified, much remains unclear regarding the mechanism by which this bacterium colonizes, invades, and disseminates within its host.
We study the mechanisms by which P. aeruginosa causes disease, with special emphasis on the set of toxins transported by the type III secretion system. These toxins orchestrate an intimate interaction between the bacterium and the host cell that results in injury or death at the cellular level and the pathophysiological entities of pneumonia, bloodstream infections, and urinary tract infections in the host. Molecular, genetic, and biochemical approaches are used in conjunction with tissue culture and animal models to better define these interactions, their impact on the innate immune response, and their implications for disease severity.
Feltman, H., G. Schulert, S. Khan, M. Jain, L. Peterson, and A. R. Hauser. 2001. Prevalence of Type III Secretion Genes in Clinical and Environmental Isolates of Pseudomonas aeruginosa. Microbiology 147:2651-2658.
Hauser, A. R., E. Cobb, M. Bodi, D. Mariscal, J. Valles, J. N. Engel, and J. Rello. 2002. Type III protein secretion is associated with poor clinical outcomes in patients with ventilator-associated pneumonia caused by Pseudomonas aeruginosa. Crit. Care Med. 30:521-528.
Rabin, S. D. P. and A. R. Hauser. 2003. Pseudomonas aeruginosa ExoU, a toxin transported by the type III secretion system, kills Saccharomyces cerevisiae. Infect. Immun. 71:4144-4150.
Schulert, G. S., H. Feltman, S. D. P. Rabin, C. G. Martin, S. E. Battle, J. Rello, and A. R. Hauser. 2003. Secretion of the toxin ExoU is a marker for highly virulent Pseudomonas aeruginosa isolates obtained from patients with hospital-acquired pneumonia. J. Infect. Dis. 188:1695-1706.
Jain, M., D. Ramirez, R. Seshadri, J. F. Cullina, C. A. Powers, G. S. Schulert, M. Bar-Meir, C. L. Sullivan, S. A. McColley, A. R. Hauser. 2004. Type III secretion phenotypes of Pseudomonas aeruginosa strains change during infection of individuals with cystic fibrosis. J. Clin. Microbiol. 42:5229-5237.
Shaver, C. M. and A. R. Hauser. 2004. Relative Contributions of Pseudomonas aeruginosa ExoU, ExoS, and ExoT to Virulence in the Lung. Infect. Immun.72:6969-6977.
Rabin, S. D. P. and A. R. Hauser. 2005. Functional regions of the Pseudomonas aeruginosa cytotoxin ExoU. Infect. Immun. 73:573-582.
Rabin, S. D. P., J. L. Veesenmeyer, K. T. Bieging, and A. R. Hauser. 2006. A C-terminal domain targets the Pseudomonas aeruginosa cytotoxin ExoU to the plasma membrane of host cells. Infect. Immun. 74:2552-2561.
Ottman, C., L. Yasmin, M. Weyand, J. L. Veesenmeyer, M. H. Diaz, R. H. Palmer, M. S. Francis, A. R. Hauser, A. Wittinghofer, and B. Hallberg. 2007. Phosphorylation-independent interaction between 14-3-3 and Exoenzyme S: from structure to pathogenesis. EMBO J. 26:902-913.
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View Publications by Alan Hauser listed in the National Library of Medicine (PubMed). |
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