Monica Kraft
Chair, Department of Medicine
Professor, BIO5 Institute
Professor, Medicine
Primary Department
Department Affiliations
(520) 626-7174
Work Summary
Monica Kraft's research focus is in the areas of adult asthma, the role of infection in asthma and the role of the distal lung in asthma and airway remodeling.
Research Interest
Monica Kraft, MD, is chair of the Department of Medicine at the University of Arizona College of Medicine – Tucson, and the Robert and Irene Flinn Endowed Professor of Medicine.Prior to joining the UA in 2014, Dr. Kraft was at Duke University, where she served as chief of the Division of Pulmonary, Allergy and Critical Care, as the Charles C. Johnson, MD, Distinguished Professor of Medicine, and as director of the Duke Asthma, Allergy and Airway Center. As vice chair for research in the Duke University Department of Medicine from 2009-2013, Dr. Kraft implemented several important initiatives to support the department’s research endeavors and was instrumental in the re-submission and renewal of Duke’s National Institutes of Health-funded Clinical Translational Science Award (CTSA).Dr. Kraft has more than 150 publications in the areas of adult asthma, the role of infection in asthma and the role of the distal lung in asthma and airway remodeling. Her work has appeared in such prestigious publications as the Journal of the American Medical Association, The Lancet, the American Journal of Respiratory and Critical Care Medicine, the Journal of Allergy and Clinical Immunology, and Chest. Her work has been funded by the National Institutes of Health and the American Lung Association.

Publications

Ledford, J., Addison, K., Guerra, S., Rojas Quintero, J., Owen, C., Martinez, F., & Kraft, M. (2016). “Club cell secretory protein deficiency leads to altered lung function in naïve mice. Journal of Allergy and Clinical Immunology.
BIO5 Collaborators
Stefano Guerra, Monica Kraft
Dakhama, A., Kraft, M., Martin, R. J., & Gelfand, E. W. (2003). Induction of regulated upon activation, normal T cells expressed and secreted (RANTES) and transforming growth factor-beta 1 in airway epithelial cells by Mycoplasma pneumoniae. American journal of respiratory cell and molecular biology, 29(3 Pt 1), 344-51.

Mycoplasma pneumoniae infection exacerbates asthma in children and may play a role in the pathogenesis of chronic asthma. Because the airway epithelium is a preferential site for M. pneumoniae infection and a major source of the chemokine regulated on activation, normal T cells expressed and secreted (RANTES) and transforming growth factor (TGF)-beta1, we postulated that this microorganism may contribute to the disease by inducing these mediators through direct interaction with airway epithelial cells. We investigated the effects of M. pneumoniae on RANTES and TGF-beta1 production in primary cultures of normal human bronchial epithelial (NHBE) cells and small airway epithelial (SAEC) cells. Both cell types were permissive to M. pneumoniae infection in vitro, but their responses were different. TGF-beta1 was induced at higher levels in NHBE than in SAEC cultures, whereas RANTES was induced in SAEC cultures but not in NHBE cultures. These effects were attenuated by erythromycin and dexamethasone. In vitro adherence assays further indicated that the effects of erythromycin were mediated through its antimicrobial action, resulting in diminished adherence of the pathogen, whereas the effects of dexamethasone did not appear to be by inhibition of adherence. These results suggest that M. pneumoniae infection may contribute to the pathogenesis of chronic asthma at different levels of the airways, by inducing TGF-beta1 in large airways and the chemokine RANTES in small airways.

Ebner, L., He, M., Virgincar, R. S., Heacock, T., Kaushik, S. S., Freemann, M. S., McAdams, H. P., Kraft, M., & Driehuys, B. (2017). Hyperpolarized 129Xenon Magnetic Resonance Imaging to Quantify Regional Ventilation Differences in Mild to Moderate Asthma: A Prospective Comparison Between Semiautomated Ventilation Defect Percentage Calculation and Pulmonary Function Tests. Investigative radiology, 52(2), 120-127.

The aim of this study was to investigate ventilation in mild to moderate asthmatic patients and age-matched controls using hyperpolarized (HP) Xenon magnetic resonance imaging (MRI) and correlate findings with pulmonary function tests (PFTs).

Djukanović, R., Wilson, S. J., Kraft, M., Jarjour, N. N., Steel, M., Chung, K. F., Bao, W., Fowler-Taylor, A., Matthews, J., Busse, W. W., Holgate, S. T., & Fahy, J. V. (2004). Effects of treatment with anti-immunoglobulin E antibody omalizumab on airway inflammation in allergic asthma. American journal of respiratory and critical care medicine, 170(6), 583-93.

IgE plays an important role in allergic asthma. We hypothesized that reducing IgE in the airway mucosa would reduce airway inflammation. Forty-five patients with mild to moderate persistent asthma with sputum eosinophilia of 2% or more were treated with humanized monoclonal antibody against IgE (omalizumab) (n = 22) or placebo (n = 23) for 16 weeks. Outcomes included inflammatory cells in induced sputum and bronchial biopsies, and methacholine responsiveness. Treatment with omalizumab resulted in marked reduction of serum IgE and a reduction of IgE+ cells in the airway mucosa. The mean percentage sputum eosinophil count decreased significantly (p

Busse, W., & Kraft, M. (2005). Cysteinyl leukotrienes in allergic inflammation: strategic target for therapy. Chest, 127(4), 1312-26.

Systemically bioavailable leukotriene receptor antagonists (LTRAs) can reduce the essential components of allergic inflammation in allergic rhinitis (AR) and asthma by blocking cysteinyl leukotriene (CysLT) activity, resulting in a wide range of clinical effects. CysLTs, mediators, and modulators in the pathophysiology of asthma and AR are a key target for therapy because they modulate production of hemopoietic progenitor cells, survival and recruitment of eosinophils to inflamed tissue, activity of cytokines and chemokines, quantity of exhaled NO, smooth-muscle contraction, and proliferation of fibroblasts. The mechanism of action of LTRAs leads to their effects on systemic allergic inflammatory processes.