About Our Research

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.

http://mic.sgmjournals.org/cgi/content/full/147/10/2659?view=long&pmid=11577145

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.

http://iai.asm.org/cgi/content/full/71/7/4144?view=long&pmid=12819106

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.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15528719

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.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15557619

Rabin, S. D. P. and A. R. Hauser. 2005. Functional regions of the Pseudomonas aeruginosa cytotoxin ExoU. Infect. Immun. 73:573-582.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=15618197

Shaver, C. M. and A. R. Hauser. 2006. Interactions between effector proteins of the Pseudomonas aeruginosa type III secretion system do not significantly affect several measures of disease severity in mammals. Microbiology 152:143-152.

http://mic.sgmjournals.org/cgi/content/full/152/1/143?view=long&pmid=16385124

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.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=16622190

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.

 Supplemental Information

Last modified Thursday, 6/28/2007
Please send comments to Scott Jeffress - s-jeff|@northwestern.edu