Dr. David Feola
Dr. David Feola

Associate Professor

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.

Recent Publications

  • Deckman Jessica M, Kurkjian Cate J, McGillis Joseph P, Cory Theodore J, Birket Susan E, Schutzman Linda M, Murphy Brian S, Garvy Beth, Feola David J. (2016). Pneumocystis infection reprograms the activation state of pulmonary macrophages. Immunobiology,
  • Haydar Dalia C, Cory Theodore J, Feola David J. (2015). Azithromycin immune-modulatory mechanism: an effect on NFkB and STAT1 signaling pathways. Proceedings of the 44th Autumn Immunology Conference,
  • Zhang B, Bailey William A, Kopper T J, Orr M B, Feola David J, Gensel John Carib. (2015). Azithromycin drives alternative macrophage activation and improves recovery and tissue sparing in contusion spinal cord injury. Journal of Neuroinflammation, 12(1), 218-23.
  • Kang Nayon, Pauly James R, Feola David J. (2015). Effects of in utero nicotine exposure on immune responses. Proceedings of the 44th Autumn Immunology Conference,
  • Array Array, Bachmeier Harrison, Ereshefsky Benjamin, Feola David J, Martin Craig A, Burgess David S. (2015). Pharmacokinetic and Pharmacodynamics (PK/PD) of Piperacillin (PIP) in Patients on Intermittent Hemodialysis (HD). ID Week 2015,
  • Opata M M, Hollifield M L, Lund F E, Randall T D, Dunn R, Garvy Beth, Feola David J. (2015). B lymphocytes are required during the early priming of CD4+ T cells for clearance of Pneumocystis infection in mice. Journal of Immunology, 195(2), 611-20.
  • Gonzalez Rene G, Feola David J. (2015). Impact of azithromycin treatment of P. aeruginosa-induced neutrophilia. Proceedings of the Infectious Diseases Fellowship Forum,
  • Haydar Dalia C, Feola David J. (2015). The impact of arginase-1 deficiency in the immune response to P. aeruginosa pneumonia. Proceedings of the Infectious Diseases Fellowship Forum,
  • Shirey K A, Pletneva L, Lau W, Finkelman F, Feola David J, Blanco J, Vogel S N. (2014). Agents that increase alternatively activated macrophage differentiation blunt respiratory syncytial virus-mediated lung pathology. Journal of Leukocyte Biology, 13(2), 951-5.
  • Cory T J, Birket S E, Murphy Brian S, Hayes, Jr D, Anstead Michael I, Kanga Jamshed Firoze, Kuhn Robert J, Bush Heather Michele, Feola David J. (2014). Impact of azithromycin treatment on macrophage gene expression in subjects with cystic fibrosis. Journal of Cystic Fibrosis : official journal of the European Cystic Fibrosis Society, 13(2), 164-71.