Cystic Fibrosis Research and Translation Center
Cystic Fibrosis Research and Translation Center
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History


SEATTLE CFRTC BACKGROUND/HISTORY


The University of Washington School of Medicine (UWSOM) and the Seattle Children's Research Institute (SCRI) have a three-decade history of promoting translational research in Cystic Fibrosis and much of our successes have been supported by a CF Foundation Research Development Program (http://depts.washington.edu/uwcffrdp/index.html). Our ability to establish fruitful collaborations of basic and clinical scientists led to the development of inhaled tobramycin as chronic preventative therapy for patients colonized with P. aeruginosa. It remains the only FDA approved inhaled antibiotic but has led to multiple active other antimicrobial development programs. The CF research community at UWSOM has long had a focus on P. aeruginosa biology as well as early lung infection and the related host response in CF. For this reason, the CF laboratory science program has been led by a remarkable group of nationally prominent microbiologists and prokaryotic geneticists including Dr. Arnold Smith, Professor of Pediatrics, Dr. Steven Lory (currently Professor of Microbiology, Harvard Medical School), Dr. Samuel Miller, Dr. Maynard Olson (who led the effort sequencing the P. aeruginosa genome), and Dr. Colin Manoil. In addition, the recruitment of Drs. E. Peter Greenberg, Caroline Harwood, Matt Parsek, and Pradeep Singh from University of Iowa significantly enhanced the P. aeruginosa biology group in the area of quorum sensing and biofilm biology in chronic P. aeruginosa infection.

The recruitment of Dr. William Parks from Washington University in St. Louis, complemented the bacterial pathogenesis group by bringing a senior investigator focused on host acquired and innate immunity in epithelia. The CFRTC will permit these very productive programs to better collaborate and enhance ongoing research.

The UW CF Research program has historically focused upon pulmonary manifestations of CF. Because progressive lung disease is the primary cause of morbidity and mortality of patients with this genetic disorder such an emphasis is not expected. Yet, gastrointestinal, nutritional and metabolic manifestations of the illness lead to significant morbidity and likely contribute to progression of lung disease. The UW program has diversified its research base into non-pulmonary manifestations of CF and the NIDDK supported CFRTC mechanism will rapidly accelerate this process.


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