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Michael Vasil, Ph.D.

Professor of Immunology & Microbiology

12800 E. 19th Ave., RC-1 N 9132
Mail Stop 8333, Aurora, CO 80045
Phone: (303) 724-4228

Michael Vasil, Ph.D., earned his doctoral degree from the University of Texas Southwestern Medical School in 1975. He completed 2 years of postdoctoral research training at the University of Oregon School of Medicine.

Dr. Vasil joined the faculty of the University of Colorado School of Medicine Department of Microbiology in 1978.

The overall goal of my research is to define the mechanism by which the premier opportunistic bacterial pathogen (i.e. Pseudomonas aeruginosa) causes both acute (e.g. septicemia) and chronic (e.g. Cystic Fibrosis (CF) pulmonary) infections and evades conventional antimicrobial therapeutic interventions needed for the treatment of these severe, often lethal infections. We employ in vitro biochemical, molecular, genetic and cellular methods, as well as in vivo approaches with appropriate animal infection models to address key questions relating to the how the virulence determinants of P. aeruginosa, as well as those of other pathogens, have a such a profound impact on the outcome of their respective infectious diseases. I have been involved in the following key discoveries over the past three decades at the University of Colorado School of Medicine.

  1. We extensively characterized a potent extracellular protein toxin (i.e. PlcH) with phospholipase C/sphingomyelinase (PLC/SMase) activities that selectively inhibits endothelial cell angiogenesis, the key process normally required for proper wound healing, which is exceptionally problematic in diabetics (see reference 5 below) We identified and characterized additional orthologs of PlcH, in P. aeruginosa (PlcN), Mycobacterium tuberculosis, Burkholderia pseudomallei and now in Bordetella pertussis and holmesii.  We also indentified and characterized a potent inhibitor of PlcH and demonstrated its efficacy the context of a model pulmonary infection in mice.
  2. We have elucidated molecular mechanisms by which P. aeruginosa regulates iron homeostasis that is absolutely crucial for its survival in the human host and to its ability incite pathogenic effects. This includes a better understanding of how the expression of virulence determinants by P. aeruginosa is influenced by iron levels in infected hosts. For example, we recently determined that iron levels, which are relevant to those that exist in the lungs of CF patients, have a profound influence on the ability of P. aeruginosa to produce a specific type of biofilm (i.e. alginate based) characteristically seen in the lungs of CF patients chronically infected with P. aeruginosa.
  3. We characterized a novel secretory system of P. aeruginosa and other significant pathogens that is required for its ability to produce pathogenic effects in a chronic pulmonary infection model. My colleagues and I were the first to report that PlcH, and many of its orthologs, are secreted through the Twin Arginine Translocase (TAT) secretory system. This unusual secretory system is only found in bacteria and plants and is not present in any animal cells, including humans, a feature that increases its potential as a drug target. We demonstrated that deletion of the TAT genes (i.e. tatABC) resulted in a very significant decrease in inflammation and virulence (i.e. in comparison to that of the wild type parental strain and the complemented mutant) in a rat lung chronic infection model. Even more notably, we demonstrated that other pathogens secret PlcH orthologs via their TAT secretory system, as does P. aeruginosa. We therefore conclude that the TAT system would be an outstanding target for the development of novel antimicrobial agents, which could assuage virulence in a manner we had observed with our TAT deletion mutant. In that regard, based on high throughput screening of >86,000 small molecular weight compounds in duplicate, we identified and characterized at least 15 lead compounds, which at this point, specifically inhibit the function of the TAT secretory system of P. aeruginosa and B. pseudomallei. These compounds and their derivatives will be further characterized in appropriate experimental animal models. 

National Institutes of Health NIAID – MERIT Award 2003-2013 

Journals-Editorial Boards:
Infection and Immunity 1987- present;
Diagnostic Microbiology and Infectious Disease 1991 - Present
Journal of Bacteriology 2002 - present
Frontiers in Microbiology 2009 - present
Applied and Environmental Microbiology 2013 - present 

NIH Study Section Service
Ad hoc member - Bacteriology and Mycology II, 1989,1990, Bacteriology and Mycology I, 1991, 1992

Regular Member
- Bacteriology and Mycology I, 1993-1998

Special Study Sections & Program Project Review
- 1992,1993,1994,1995; NIDDK- RFA for Cystic Fibrosis, Special Study Section Member – 1996; NIH Topics in Bacterial Pathogenesis and Special Emphasis Study Sections – 2002, 2003, 2004, 2005, 2006, 2007, 2008, 2009,2010,2011,2012, 2013, 2014

Veterans Administration
Merit Review Subcommittee for Infectious Diseases 2000-2004.

Cystic Fibrosis Foundation – Member Research and Research Training Committee 1996 - Present 

Excellence in Teaching Award
- presented by the Sophomore Medical Class of the University of Colorado School of Medicine, 1984, 1986, 1987, 1992, 2001, 2002, 2003, 2004, 2005, 2007, 2010, 2012.

Elected - Academy of Medical Educators - 2011
– University of Colorado School of Medicine 

Miscellaneous Honors
Fulbright Scholarship Award - 1986.
Fellow - American Academy of Microbiology, Elected - 1990
Chair, Division D - American Society for Microbiology 1992
Fellow - Infectious Disease Society of America, Elected - 1996
Kadner Institute Faculty (American Society for Microbiology) for Graduate Students and Postdoctoral Scientists – Preparation for Careers in Microbiology 2008, 2009, 2010, 2011.