Dr. David Feola
Dr. Feola received his Doctor of Pharmacy and Philosophy degrees from the University of Kentucky College of Pharmacy. He also completed residencies in pharmacy practice and infectious diseases pharmacotherapy at the UK Chandler Medical Center (R258). His primary research focus area is immunology and infectious diseases pharmacotherapy, with specific projects investigating immunomodulatory and immunotoxic properties of drug exposure in animals and humans. Dr. Feola is building a translational research program through which he utilizes animal models and molecular and cellular investigations to generate investigator-initiated of clinical trials. He conducts a research program focused on mechanistic and translational investigations to define the role of alternatively activated macrophages in the pathophysiology of pulmonary fibrosis. This is accomplished through the use of a mouse model of Pseudomonas aeruginosa (PA) infection and through clinical studies in patients with cystic fibrosis. The goal of this research is to improve the understanding of chronic inflammatory lung diseases and to help identify potential therapeutic targets to slow the progression of chronic inflammation and tissue remodeling. Alternatively activated macrophages are involved in the promotion of Th2-type immune responses, debris scavenging, tissue remodeling, and fibrosis. These cells have also been shown to inhibit both Th1-type responses and the function of classically activated macrophages responsible for the initiation and propagation of inflammation. In a series of randomized, clinical trials, azithromycin (AZM) has been shown to favorably impact morbidity and mortality in CF patients infected with PA. His group recently demonstrated that AZM will polarize macrophages to an M2-like phenotype both in vitro when stimulated with LPS and IFN and in a mouse model of pulmonary PA infection. Although M2 cells have been examined in Th2-dominated settings, the role of this cell type in the response to gram-negative bacterial infection has not been studied. The main hypothesis of this work is that polarization of the macrophage response toward the alternative phenotype will limit inflammation and alter the subsequent fibrosis caused by PA infection Other projects in the lab include: combined immunotoxicity of zidovudine plus sulfamethoxazole-trimethoprim exposure, the control of T lymphocyte expansion and memory generation by cognate interactions with B cells, and the effect of antimicrobial agents on quorum sensing gene expression in Staphylococcus aureus. Dr. Feola also coordinates the infectious diseases module in the Advanced Therapeutics course for the Doctor of Pharmacy Program, and provides clinical service to the Infectious Diseases inpatient consult team at the UK Chandler Medical Center.