Bradley H. Rosen, DO, Associate of Internal Medicine in Pulmonary, Critical Care, and Occupational Medicine, has joined the KL2 Scholars program, which is designed to provide intensive curricular and mentoring support for postdoctoral researchers. Earlier this year, the University of Iowa Institute for Clinical and Translational Science renewed the KL2 Career Development Award. Dr. Rosen was one of four selected to participate in this three-year program, which will fund a significant portion of his salary and cover most of his tuition, travel, and supplies costs for the duration.
As a KL2 Scholar, Dr. Rosen’s next three years will combine the above research with PhD-graduate-level coursework that will help him gain additional understanding of molecular biology. He will also receive mentoring and career development guidance from Dr. John Engelhardt and Pulmonary Division Director Dr. Joseph Zabner. The goal of the KL2 program is for Scholars to develop successful clinical and translational research careers such that they become competitive for higher-level independent grants from the National Institutes of Health. Dr. Zabner praised the growth Dr. Rosner has already shown. “After finishing his fellowship, Dr. Rosen chose to remain at the University of Iowa because of his commitment to a career in translational research, spending three years as a postdoctoral fellow in the Pulmonary T32 training program.”
Dr. Rosen will continue his study of cystic fibrosis (CF) lung disease in Dr. Engelhardt’s laboratory. His recent work in the Cystic Fibrosis Transmembrane Regulator (CFTR)-null ferret model demonstrates that, while infection can be prevented using preemptive lifelong antibiotics, mucoinflammatory lung disease still develops. However, this occurs at a slower pace when compared with CF animals given conventional symptom-triggered antibiotic therapy. This suggests that, in the absence of functional CFTR, there is an innate and inevitable tendency toward lung disease and that infection accelerates this process. Based on these results Dr. Rosen will build on the hypothesis that in CF, dysregulated mucin subtypes contribute to the initiation and propagation of mucoinflammatory lung disease. He will test this using novel transgenic ferrets and a CRISPR/Cas9 gene-editing approach in airway stem cell cultures. Because excess and persistent mucus is a feature of other lung diseases such as COPD and asthma, Dr. Rosen’s discoveries in this work may help further understanding of these conditions as well and inform new approaches for treatment.
For more information about the KL2 Scholars program: https://icts.uiowa.edu/workforce-development/kl2-scholars-program