Division of Pulmonary and Critical Care Medicine

		Lynn M. Schnapp, M.D. Associate Professor of Medicine Pulmonary and Critical Care Medicine OFFICE ADDRESS Harborview Medical Center 325 Ninth Avenue, Box 359640 Seattle, WA 98104 lschnapp@u.washington.edu Academic Office: (206) 341-5389 Fax: (206) 341-5392
EDUCATION AND TRAINING B.S., Massachusetts Institute of Technology Cambridge, MA, 1978-1982. M.D., University of Pennsylvania, Philadelphia, PA, 1982-1986. Residency in Internal Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA, 1986-1989. Fellowship in Pulmonary and Critical Care Medicine, University of California, San Francisco, San Francisco, CA, 1989-1992.		CURRENT RESEARCH INTERESTS The focus of the laboratory is on the role of integrins, a class of adhesion molecules, and extracellular matrix proteins in normal and pathological conditions. In particular, we are interested in the processes that govern acute lung injury and its resolution. We previously identified and characterized a new integrin (alpha 8) that is expressed in alveolar myofibroblasts, is upregulated in pulmonary fibrosis, and mediates cell survival. We hypothesize that inhibition of myofibroblast apoptosis following lung injury will slow the spontaneous resolution of fibrosis. To test this, we have developed mouse models of bleomycin-induced lung injury to examine the role of the alveolar myofibroblasts and integrins in resolution of fibrosis. In a related project, we are developing new methodologies in proteomics to analyze BAL fluid from ARDS patients in collaboration with Reudi Aebersold (Institute of Systems Biology). This approach will allow us to identify new pathways in lung injury and develop prediction models for the outcome of lung injury in patients. Another focus in the laboratory is to characterize the interactions of the extracellular environment with HIV in the lung. The lung is an important reservoir of HIV and site of HIV replication, which results in virus-induced lung injury. How HIV leads to direct lung injury, and how virus replication is sustained within the lung, are not known. We hypothesize that extracellular matrix (ECM) enhance and sustain IV infection within the lung and, conversely, that HIV within the lung alters ECM and contributes to inflammation and fibrosis. REPRESENTATIVE PUBLICATIONS Pal S, Schnapp LM. HIV-infected lymphocytes regulate fibronectin synthesis by TGF beta 1 secretion. J Immunol. 172(5):3189-95, 2004 Wagner TE, Frevert CW, Herzog EL, Schnapp LM. Expression of the integrin subunit alpha 8 in murine lung development. J Histochem Cytochem 51(10):1307-15, 2003. Lu M, Munger J, Busald C, Shao L, Schnapp LM. The integrin alpha 8 beta 1 mediates adhesion to LAP-TGF beta 1. J cell Sci 115(23):4641-8, 2002. Levine DM, Rockey D, Milner TA, Breuss JM, Fallon JT, Schnapp LM. Expression of the integrin alpha 8 beta 1 during pulmonary and hepatic fibrosis. Am J Path. 156:1927-1935, 2000.

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