Assistant Professor
Dept of Clinical Pharmacy

MEMPHIS TN 381631980
Tel: (901) 448-7216


  • PostDoc, University of Nebraska Medical Center, Omaha, NE, Pharmacokinetics
  • Ph.D., University of Kentucky, Lexington, KY, Pharmaceutical Sciences
  • Pharm.D., Drake University, Des Moines, IA, Pharmacy

Research Interest/Specialty


Clinical Pharmacology

Macrophage immunology

Research Description

 Modern antiretroviral therapy is capable of reducing levels of HIV-1 to below detectable levels in a large percentage of HIV+ individuals in the plasma.  These individuals, however, are not cured of HIV.  The virus is capable of hiding inside of cells in a number of sites of immune privilege referred to as reservoir or sanctuary sites.  In these sites, drug concentrations appear to be subtherapeutic, preventing the drugs from being able to fully inhibit replication.  One of the key cells in these sites are macrophages.

Macrophages can be polarized to one of two subsets.  The first, the M1 or classically activated macrophage is pro-inflammatory and involved in the clearance of acute infections.  The second, the M2 or alternatively activated macrophage is anti-inflammatory and predominantly involved in tissue repair.  The role of these macrophage subsets as reservoirs for HIV is currently unknown.  I aim to elucidate differences in intracellular antiretroviral concentrations between these two subsets of macrophages, as a means to try to determine methods to increase drug concentrations inside of sanctuary sites throughout the body.

Research Keywords

  • HIV
  • Pharmacokinetics
  • Clinical Pharmacology
  • Macrophage Immunology
  • Sanctuary/Reservoir Sites


  1. Estes, JD, Reilly, C, Trubey, CM, Fletcher, CV, Cory, TJ, Piatak, M, Russ, S, Anderson, J, Reimann, TG, Star, R, Smith, A, Tracy, RP, Berglund, A, Schmidt, T, Coalter, V, Chertova, E, Smedley, J, Haase, AT, Lifson, JD, Schacker, TW. Antifibrotic Therapy in Simian Immunodeficiency Virus Infection Preserves CD4+ T-Cell Populations and Improves Immune Reconstitution With Antiretroviral Therapy. J Infect Dis, 2014.
  2. Cory, TJ, Birket, SE, Murphy, BS, Hayes, D, Anstead, MI, Kanga, JF, Kuhn, RJ, Bush, HM, Feola, DJ. Impact of azithromycin treatment on macrophage gene expression in subjects with cystic fibrosis. J Cyst Fibros, 13 (2), 164-71, 2014.
  3. Cory, TJ, Schacker, TW, Stevenson, M, Fletcher, CV. Overcoming pharmacologic sanctuaries. Curr Opin HIV AIDS, 8 (3), 190-5, 2013.
  4. Cory, TJ, Birket, SE, Murphy, BS, Mattingly, C, Breslow-Deckman, JM, Feola, DJ. Azithromycin increases in vitro fibronectin production through interactions between macrophages and fibroblasts stimulated with Pseudomonas aeruginosa. J Antimicrob Chemother, 68 (4), 840-51, 2013.
  5. Sabeva, NS, McPhaul, CM, Li, X, Cory, TJ, Feola, DJ, Graf, GA. Phytosterols differentially influence ABC transporter expression, cholesterol efflux and inflammatory cytokine secretion in macrophage foam cells. J Nutr Biochem, 22 (8), 777-83, 2011.
  6. Murphy, BS, Bush, HM, Sundareshan, V, Davis, C, Hagadone, J, Cory, TJ, Hoy, H, Hayes, D, Anstead, MI, Feola, DJ. Characterization of macrophage activation states in patients with cystic fibrosis. J Cyst Fibros, 9 (5), 314-22, 2010.
  7. Feola, DJ, Garvy, BA, Cory, TJ, Birket, SE, Hoy, H, Hayes, D, Murphy, BS. Azithromycin alters macrophage phenotype and pulmonary compartmentalization during lung infection with Pseudomonas. Antimicrob Agents Chemother, 54 (6), 2437-47, 2010.
  8. Murphy, BS, Sundareshan, V, Cory, TJ, Hayes, D, Anstead, MI, Feola, DJ. Azithromycin alters macrophage phenotype. J Antimicrob Chemother, 61 (3), 554-60, 2008.
  9. Fogarty, BA, Heppert, KE, Cory, TJ, Hulbutta, KR, Martin, RS, Lunte, SM. Rapid fabrication of poly(dimethylsiloxane)-based microchip capillary electrophoresis devices using CO2 laser ablation. Analyst, 130 (6), 924-30, 2005.