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
Walter, M. J., Castro, M., Kunselman, S. J., Chinchilli, V. M., Reno, M., Ramkumar, T. P., Avila, P. C., Boushey, H. A., Ameredes, B. T., Bleecker, E. R., Calhoun, W. J., Cherniack, R. M., Craig, T. J., Denlinger, L. C., Israel, E., Fahy, J. V., Jarjour, N. N., Kraft, M., Lazarus, S. C., , Lemanske, R. F., et al. (2008). Predicting worsening asthma control following the common cold. The European respiratory journal, 32(6), 1548-54.

The asthmatic response to the common cold is highly variable, and early characteristics that predict worsening of asthma control following a cold have not been identified. In this prospective multicentric cohort study of 413 adult subjects with asthma, the mini-Asthma Control Questionnaire (mini-ACQ) was used to quantify changes in asthma control and the Wisconsin Upper Respiratory Symptom Survey-21 (WURSS-21) to measure cold severity. Univariate and multivariable models were used to examine demographic, physiological, serological and cold-related characteristics for their relationship to changes in asthma control following a cold. Clinically significant worsening of asthma control was observed following a cold (mean+/-SD increase in mini-ACQ score of 0.69+/-0.93). Univariate analysis demonstrated that season, centre location, cold duration and cold severity measurements were all associated with a change in asthma control. Multivariable analysis of the covariates available within the first 2 days of cold onset revealed that the day 2 and cumulative sum of day 1 and 2 WURSS-21 scores were significant predictors of the subsequent changes in asthma control. In asthmatic subjects, cold severity within the first 2 days can be used to predict subsequent changes in asthma control. This information may help clinicians prevent deterioration in asthma control following a cold.

Kraft, M., Cassell, G. H., Pak, J., & Martin, R. J. (2002). Mycoplasma pneumoniae and Chlamydia pneumoniae in asthma: effect of clarithromycin. Chest, 121(6), 1782-8.

To determine the effect of clarithromycin therapy in patients with asthma.

Fouty, B., Moss, T., Solodushko, V., & Kraft, M. (2006). Dexamethasone can stimulate G1-S phase transition in human airway fibroblasts in asthma. The European respiratory journal, 27(6), 1160-7.

Corticosteroids are the first line of therapy for asthma. Whether they alter the progression of airway remodelling in asthma is, as yet, unknown. To determine whether corticosteroids could alter the fibroblast cell cycle the current authors studied the effect of dexamethasone on cultured airway fibroblasts obtained from nine mild-to-moderate, steroid-naïve asthmatics (forced expiratory volume in one second 78+/-4% predicted), and seven normal controls. Fibroblasts were cultured from endobronchial biopsies obtained via bronchoscopy. Cells were exposed to dexamethasone (10(-9)-10(-7) M) and studied at 72 h to determine differences in progression through the cell cycle. In asthmatic fibroblasts, dexamethasone, at concentrations of 10(-8)M and 10(-7)M, nearly doubled the number of cells in the S phase (17.8+/-3.0% and 18.4+/-3.1%, respectively) compared with untreated fibroblasts (10.3+/-1.4%). There was no significant effect in normal control fibroblasts. Dexamethasone induced hyperphosphorylation of the tumour suppressor, retinoblastoma (RB) in asthmatic fibroblasts; fibroblasts from normal controls had significantly less hyperphosphorylation of RB. No difference in protein expression of the CCAAT/enhancer binding protein alpha between the two groups was detected. This study suggests that dexamethasone can stimulate G1-S phase cell cycle transition in human airway fibroblasts obtained from asthmatics. Whether this leads to enhanced airway remodelling in some individuals remains to be determined.

Kraft, M. (1999). The distal airways: are they important in asthma?. The European respiratory journal, 14(6), 1403-17.

Although the airways of