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Stephen
Tilley
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Degrees BA: (1988) University of North Carolina, Chapel Hill, N.C. MD: (1992) University of North Carolina, Chapel Hill, N.C. Residency: (1995) Vanderbilt University, Nashville, TN Fellowship (2000) University of North Carolina, Chapel Hill, N.C. |
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| Clinical Interests: Sarcoidosis, Asthma, General Pulmonary Medicine, Critical Care Research Interests: The primary role of the human immune system is protection against infection. Sometimes, however, our immune system becomes "hyperactive" for unclear reasons resulting in unwanted inflammation. Asthma and sarcoidosis are two diseases which effect the lungs and are felt to be caused by such an exaggerated immune response. These diseases represent two opposing ends of the immunological spectrum, with asthmatic inflammation consisting of specific cell types and inflammatory mediators and sarcoidal inflammation consisting of different cell types and alternative inflammatory mediators. The development of each of these types of immune response tends to down-regulate the other, making the study of both diseases complimentary. Since it is impossible to carry out an in depth study of the immune system in humans with sarcoidosis and asthma, we are utilizing well-established animal models of disease. In these models we are incorporating genetic approaches to dissect the roles of certain inflammatory mediators as they contribute the initiation, propagation, and resolution of lung inflammation. Further understanding of these processes may lead to the development of new drugs which more specifically target the factors contributing to the exaggerated immune response seen in these diseases. |
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Bhattacherjee P, Mukhopadhyay P, Tilley SL, Koller BH, Geoghgan T, Paterson CA. Blood-aqueous barrier in prostaglandin EP2 receptor knockout mice. Ocular Immunology & Inflammation. In Press. 2003. Tilley SL, Tsai M, Williams CM, Wang Z-S, Erikson CJ, Galli SJ, Koller BH. Identification of A3 receptor- and mast cell-dependent and -independent components of adenosine-mediated airway responsiveness in mice. J Immunol. In Press. 2003. Zhong H, Shlykov SG, Molina JG, Sanborn BM, Jacobson MA, Tilley SL,
Blackburn MR. Activation of murine lung mast cells by the adenosine A3
receptor. J Immunol. In Press. 2003. Tilley SL, Hartney JM, Erikson Cj, Jania C, Nguyen M, Stock J, McNeisch J, Valancius C, Panetteri RA Jr, Penn Rb, Koller BH. Receptors and pathwasy mediating the effects of prostaglandin E2 on airway tone. Am J Physiol Lung Cell Mol Physiol. 284(4):L599-606. April 2003. Nguyen M, Solle M, Audoly LP, Tilley SL, Stock JL, McNeish JD, Coffman TM, Dombrowicz D, Kolley BH. Receptors and signaling mechanisms required for prostaglandin E2-mediated regulation of mast cell degranulation ad IL-6 production. J Immunol. 169(8):4586-93. October 2002. Tilley SL, Coffman TM, Koller BH. Mixed messages: modulation of inflammation and immune responsees by prostaglandins and thromboxanes. J Clin Invest. 108(1):15-23. July 2001. Nataraj C, Thomas DW, Tilley SL, Nguyen MT, Mannon R, Koller BH, Coffman TM. Receptors for prostaglandin E(2) that regulate cellular immune responses in the mouse. J Clin Invest. 108(8):1229-35. October 2001. Audoly LP, Ruan X, Wagoner VA, Goulet JL, Tilley SL, Koller BH, Coffman TM, Arendshorst WJ. The role of EP2 and EP3 prostaglandin E2 receptors in the control of murine renal hemodynamics. Am. J. Physiol. 280(1):H327-33. January 2001. Tilley SL, Wagoner VA, Salvatore CA, Jacobson MA, Koller BH. Adenosine
and inosine Salvatore CA, Tilley SL, Fletcher D Latour AM, Fletcher DS, Koller BH, Jacobson, MA. Disruption of the A3 adenosine receptor gene in mice and its effect on stimulated inflammatory cells. J. Biol. Chem. 275: 4429-4434. February 2000. Tilley SL, Audoly LP, Hicks EH, Kim A, Coffman TM, Koller BH. Reproductive failure and reduced blood pressure in mice deficient in the EP2 PGE2 receptor. J. Clin Invest. 103:1539-1545. June 1999. Audoly LP, Tilley SL, Goulet J, Key M, Nguyen M, Stock JL, McNeish
JD, Koller BH, Coffman TM.
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