Stokes Peebles, M.D.

Professor of Medicine, Division of Allergy, Pulmonary and Critical Care Medicine
Elizabeth and John Murray Chair in Medicine
Training Program Director, Allergy Immunology Fellowship Program
Professor of Pathology, Microbiology and Immunology
T-1218 MCN Vanderbilt University Medical Center
1161 21st Avenue South

Allergically-mediated and virally-induced lung inflammation

Dr. Stokes Peebles is John and Elizabeth Murray Professor of Medicine at Vanderbilt University Medical School. He graduated with an M.D. degree from Vanderbilt in 1986, was a resident in internal medicine at Vanderbilt, and was elected to the Alpha Omega Alpha Honor Medical Society. 

Dr. Peebles performed a four year fellowship in Allergy/Clinical Immunology at Johns Hopkins School of Medicine (1991-1995) and then returned to Vanderbilt where he completed a three year fellowship in Pulmonary/Critical Care Medicine (1995-1998). 

He is Board Certified in Internal Medicine, Allergy/Immunology, Pulmonary, and Critical Care. Dr. Peebles has a very active research program examining the role of eicosanoids in allergic and virally-induced lung inflammation for which he has been supported by the American Academy of Allergy, Asthma, and Immunology Education Research Trust Award and the National Institutes. 

Research Information

The Peebles Lab investigates mechanisms regulating lung inflammation, with specific emphasis on allergen-induced and virus-mediated disease. Allergic airway inflammation is one of the most common diseases in both children and adults, and is a strong predisposing factor for the development of asthma. Viral infections are causative in approximately 80% of children and 50% of adults. Our lab has a particular interest in the interaction of allergic disease and respiratory syncytial virus in causing airways responsiveness. While we are interested in study host immune responses to both allergens and viruses, we are particularly interested in the contribution of group 2 innate lymphoid cells (ILC2) as an initiator of lung inflammatory responses. Additionally, our lab has a long-standing interest in how prostaglandins, particularly PGI2, regulate lung inflammatory responses. We are currently determining how PGI2 controls T regulatory (Treg) cell function in several models of inflammation. We have developed a variety of tools to understand how both endogenous and exogenous prostaglandin signaling modulates both allergen-induced and virus-induced pulmonary inflammation. Lastly, we are now investigating how glucagon-like peptide-1 signaling regulates lung inflammation, as a possible treatment for asthma in the setting of obesity.

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