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.


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
Lugogo, N. L., Kraft, M., & Dixon, A. E. (2010). Does obesity produce a distinct asthma phenotype?. Journal of applied physiology (Bethesda, Md. : 1985), 108(3), 729-34.

Obesity and asthma prevalence have been increasing over the past decade. Epidemiological evidence demonstrates that obesity results in an increased risk of developing incident asthma. Even modest levels of increased weight increase asthma risk. Recently published data suggest that obese asthma patients may represent a distinct phenotype of asthma. Obese asthma patients demonstrate increased asthma severity, as indicated by increased exacerbations and decreased asthma control; however, they do not appear to have increased airway cellular inflammation. It seems likely that obesity does not contribute to asthma through conventional Th type 2-mediated inflammatory pathways but, rather, through separate mechanisms that are specific to the obese state. This may explain the variable responses of obese asthma patients to conventional asthma therapies, specifically, relative corticosteroid resistance. Small studies suggest improvements in the disease with weight loss in obese asthma patients, and other interventions to target asthma in obese individuals need to be investigated. Several postulated mechanisms for the occurrence of this distinct phenotype have been postulated: 1) the presence of comorbidities, such as gastroesophageal reflux disease and sleep disordered breathing, 2) systemic inflammation associated with obesity (with elevated levels of circulating cytokines, such as IL-6 and TNF-alpha), 3) increased oxidative stress, and 4) hormones of obesity, such as adiponectin, leptin, and resistin. Although the mechanisms underlying obesity in asthma require further investigation, obesity plays a major role in the asthma epidemic and likely results in a distinct phenotype of the disease.

Sutherland, E. R., Martin, R. J., Ellison, M. C., & Kraft, M. (2002). Immunomodulatory effects of melatonin in asthma. American journal of respiratory and critical care medicine, 166(8), 1055-61.

Patients with nocturnal asthma demonstrate circadian variations in airway inflammation. We hypothesized that melatonin, a circadian rhythm regulator, modulates circadian inflammatory variations in asthma. The effect of melatonin stimulation on peripheral blood mononuclear cell cytokine production was evaluated at 4:00 P.M. and 4:00 A.M. in normal control subjects, patients with nocturnal asthma, and patients with non-nocturnal asthma. Melatonin was proinflammatory, causing significantly increased production of interleukin-1, interleukin-6, and tumor necrosis factor-alpha at 4:00 P.M. and 4:00 A.M. in all subject groups (range, 12.8 +/- 3.3 to 131.72 +/- 16.4%, p 0.05, both cases). At 4:00 P.M., the cytokine response to melatonin of patients with nocturnal asthma was greater than that of control subjects or patients with non-nocturnal asthma and did not change significantly at 4:00 A.M. At 4:00 P.M., the cytokine response of patients with non-nocturnal asthma was less than that of patients with nocturnal asthma and rose significantly at 4:00 A.M. (p = 0.0001, all comparisons). Melatonin is proinflammatory in both patients with asthma and healthy subjects. Patients with nocturnal asthma demonstrate the largest daytime cytokine response and cannot be further stimulated at 4:00 A.M., suggesting chronic overstimulation in vivo. These results suggest differential immunomodulatory effects of melatonin based on asthma clinical phenotype and may indicate an adverse effect of exogenous melatonin in asthma.

Sutherland, E. R., Ellison, M. C., Kraft, M., & Martin, R. J. (2003). Altered pituitary-adrenal interaction in nocturnal asthma. The Journal of allergy and clinical immunology, 112(1), 52-7.

Increased airway inflammation at night contributes to the nocturnal worsening of asthma, but the mechanisms regulating circadian variations in airway inflammation are unknown.

Denlinger, L. C., Manthei, D. M., Seibold, M. A., Ahn, K., Bleecker, E., Boushey, H. A., Calhoun, W. J., Castro, M., Chinchili, V. M., Fahy, J. V., Hawkins, G. A., Icitovic, N., Israel, E., Jarjour, N. N., King, T., Kraft, M., Lazarus, S. C., Lehman, E., Martin, R. J., , Meyers, D. A., et al. (2013). P2X7-regulated protection from exacerbations and loss of control is independent of asthma maintenance therapy. American journal of respiratory and critical care medicine, 187(1), 28-33.

The function of the P2X(7) nucleotide receptor protects against exacerbation in people with mild-intermittent asthma during viral illnesses, but the impact of disease severity and maintenance therapy has not been studied.