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Michael J. Schurr, Ph.D.

Associate Professor of Immunology & Microbiology

12800 E. 19th  Ave., RC-1 N 9113
Mail Stop 8333, Aurora, CO 80045
Phone: (303) 724-4221

Michael Schurr, Ph.D., earned his doctoral degree from the University of North Texas in 1992. He completed 4 years of postdoctoral research training at the University of Texas Health Sciences Center in San Antonio.

Before joining the faculty of the University of Colorado School of Medicine Department of Microbiology in 2006, Dr. Schurr served on the faculty of the University of Michigan School of Medicine and Tulane University Health Science Center.

The focus of research efforts in my laboratory is on the pathogenic mechanisms of Pseudomonas aeruginosa, specifically in cystic fibrosis (CF) chronic respiratory infections. The leading cause of morbidity and mortality in CF is due to complications of chronic P. aeruginosa infection. P. aeruginosa is a Gram-negative soil and water microorganism that is capable of causing a plethora of different infections in patients whose innate immune systems have been compromised by either treatment or disease. In CF, many different environmental and host immune factors affect P. aeruginosa such that a majority of the organisms isolated from these patient’s lungs over time exhibit an altered phenotype termed mucoidy. Mucoidy is the direct result of over-producing the exopolysaccharide alginate that allows the organism to hide from the immune system and quench reactive oxygen intermediates. My laboratory is focused on one of the first transcriptional regulators identified to be important for the mucoid phenotype, AlgR, as it appears to be a global regulator of virulence in P. aeruginosa. We have been able to show that AlgR controls at least five different virulence determinants (alginate, pyoverdin, pili function, chemotaxis and HCN production) in P. aeruginosa. We have focused on HCN production, its role in P. aeruginosa pathogenesis and the role of AlgR in its production. We have observed that a majority (86%) of clinical CF P. aeruginosa isolates produced elevated amounts of HCN. In addition, we have discovered that AlgR and AlgZ control this process and these two proteins are likely operating as a two-component regulatory system. This may have significant implications for future therapeutics for P. aeruginosa as well as other bacterial pathogens.

Another interesting dimension is that our data indicates that mucoid P. aeruginosa may be producing HCN in biofilms. There is ample evidence that P. aeruginosa exists as a biofilm in CF patient lungs. However, the virulence of clinical CF P. aeruginosa isolates is greatly reduced. Our data indicates that P. aeruginosa may be actively making HCN in these biofilms and hence in the lungs of CF patients.

We also examine factors governing host-pathogen interactions with both the microbes and the host being examined at different levels using tools spanning areas from genetics to cell biology. The ongoing investigations are in the following areas: (i) stress response in P. aeruginosa; (ii) the relationship between stress response and inflammation and; (iii) animal models of respiratory infection in normal and transgenic mice.

Dr. Schurr received a New Investigator Award from the Cystic Fibrosis Foundation.  He has been a reviewer for numerous grants study sections and journals.