Jennifer L. Taylor-Cousar,
MD
Assistant Professor,
Adult CF Program
Director/Associate CF
Center Director,
Departments of Internal
Medicine and Pediatrics,
Pulmonary Division
Education and Honors:
1993, B.A., Human Biology, Stanford University, Stanford, CA; 1998, M.D., Duke University
Medical Center, Durham, NC; 2002, Internship and Residency, Internal Medicine and Pediatrics,
Duke University Medical Center; 2006, Fellowship, Adult and Pediatric Pulmonary Medicine,
Duke University Medical Center; 1994-1998, Dean’s Tuition Scholar, Duke University Medical
Center; 1996-1997, Four Schools Physician Scientist Research Scholar, Duke University Medical
Center; 2001, Huber Scholar, Duke University Medical Center International Health Program;
2003-2004, Cystic Fibrosis Foundation Clinical Fellow, Duke University Medical Center; 2006,
Pulmonary Fellowship Scientific Achievement Award Duke University Medical Center; 2008,
Clinical Trials Center New Investigator of the Year Award
Research Interests:
My research interests are infection and innate immunity in cystic fibrosis lung disease. Based on
work in CF cells, investigators have shown that CFTR specific dysfunction may be correctable
with administration of phosphodiesterase inhibitors (PDEi) 1-3 In addition, laboratory studies in cell
lines and animals indicate that PDEi such as sildenafil may have anti-inflammatory activity.4
Furthermore, recent studies have shown that PDEi (and a PDEi analog) can correct localization
of CFTR, and potentiate CFTR-mediated chloride activity. 2,3 Finally, in a case report of sildenafil
in a patient with severe CF lung disease and secondary pulmonary hypertension worsened by
exercise showed that the drug was efficacious and well tolerated. 5 Thus, phosphodiesterase
inhibitors may provide a therapeutic drug class that will address multiple aspects of CF lung
disease. In order to determine safety, pharmacokinetics and mechanism of effect of sildenafil in
CF, I will be conducting two separate pilot studies. The first will examine pharmacokinetics,
safety and effect of PDEi on sputum and exhaled breath biomarkers of inflammation. The second
will examine the in vivo effect of sildenafil on CFTR function as measured by electrolyte transport
in the nasal epithelium and in the sweat ducts. The long-term goal of this research is to translate
the information learned about the pathophysiology of CF lung disease from work in CF cells to
efficacious therapeutic options for CF patients.
Publications:
Carraway MS, Ghio AJ, Taylor JL, and Piantadosi CA. Lung Specific Induction of ferritin and
hemeoxygenase-1 by endotoxin in the lung. American Journal of Physiology. 1998;275(3 pt
1):L583-92.
Taylor JL, Carraway MS, and Piantadosi CA. Lung Specific Induction of Heme Oxygenase-1
and Hyperoxic Lung Injury. American Journal of Physiology. 1998; 274(4 pt 1):L582-90.
Taylor JL, Quiñones Maymí DM, Sporn TM, McAdam HP, and Wahidi MW. Multiple Lung
Nodules in a Woman with a history of Melanoma. Respiration. 2003;70:544-48.
Ole-Nguyaine S, Crump JA, Kibiki GS, Kiang K, Taylor J, Schimana W, Bartlett JA, Shao JF, and
Thielman NM. HIV-associated morbidity, mortality, and diagnostic testing opportunities among
inpatients at a referral hospital in northern Tanzania. Annals of Tropical Medicine and
Parasitology. 2004;98(2):171-9.
Taylor JL and SM Palmer. Mycobacterial Abscessus Chest Wall and Pulmonary Infection in a
Cystic Fibrosis Lung Transplant Recipient. Journal of Heart and Lung Transplantation. 2006
25:985-8.
Taylor JL, and SM Palmer.
A Critical Care Perspective on Immunotherapy in Lung
Transplantation. Journal of Intensive Care Medicine. 2006; 21(6):327-344.
Poschet J, Timmins G, Taylor-Cousar JL, Ornatovski W, Fazio J, Perkett E, Wilson K, Yu HD,
de Jonge HR and Deretic V. Pharmacological modulation of cGMP levels by Phosphodiesterase
5 Inhibitors as a Therapeutic Strategy for Treatment of Respiratory Pathology in Cystic Fibrosis.
Am J Physiol Lung Cell Mol Physiol. 2007;293:L12-L19.
Ornatowski W, Poschet JF, Perkett E, Taylor-Cousar JL and Deretic V. Hypersusceptibility to
Pseudomonas aeruginosa Exotoxin A Due to Elevated Furin in Cystic Fibrosis Respiratory
Epithelial Cells. J Clin Invest. 2007;117:3498-3506.
Taylor-Cousar JL, Zariwala MA, Burch LH, Pace RG, Drumm ML, Calloway H, Fan H, Weston
BW, Wright FA, Knowles MR. Histo-blood Group Gene Polymorphisms as Potential Genetic
Modifiers of Infection and Cystic Fibrosis Lung Disease Severity.
PLoSOne.
2009
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0004270
Bibliography:
1.
Poschet JF, Fazio JA, Timmins GS, et al. Endosomal hyperacidification in cystic fibrosis
is due to defective nitric oxide-cylic GMP signalling cascade. EMBO Rep 2006;7(5):553-9.
2.
Dormer RL, Harris CM, Clark Z, et al. Sildenafil (Viagra) corrects DeltaF508-CFTR
location in nasal epithelial cells from patients with cystic fibrosis. Thorax 2005;60(1):55-9.
3.
Cobb BR, Fan L, Kovacs TE, Sorscher EJ, Clancy JP. Adenosine receptors and
phosphodiesterase inhibitors stimulate Cl- secretion in Calu-3 cells. Am J Respir Cell Mol Biol
2003;29(3 Pt 1):410-8.
4.
Toward TJ, Smith N, Broadley KJ. Effect of phosphodiesterase-5 inhibitor, sildenafil
(Viagra), in animal models of airways disease. Am J Respir Crit Care Med 2004;169(2):227-34.
5.
Montgomery GS, Sagel SD, Taylor AL, Abman SH. Effects of sildenafil on pulmonary
hypertension and exercise tolerance in severe cystic fibrosis-related lung disease. Pediatr
Pulmonol 2006;41(4):383-5.