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My laboratory is interested in the study of the immune response to various environmental insults (including respiratory viral infections, diesel particle exposure, and allergen exposure) in neonates and their link to the development of adult airway inflammation, asthma.

The occurrence of inflammatory respiratory diseases, such as asthma, has increased dramatically in the past decade approaching epidemic levels among the peoples of industrialized countries. Although a genetic basis for this disease state has been suggested, environmental factors are partly responsible for the rising trend. A major step forward in our understanding of asthma will occur when more is known about the gene-environmental interactions and how they manifest into airway disease. An ever-increasing number of studies have begun to suggest that early exposure to various environmental insults orchestrate many of the events critical to the development of asthma. The objective of my laboratory is to realize the initiators of the immune and pathophysiological changes that occur during the early stages of pulmonary airways disease and ultimately to understand the fundamental causes of asthma so that more effective interventions and therapy might be developed.

Our immediate goal is to determine if exposure during early neonatal life to environmental factors leads to predisposition, development of, or exacerbation of allergic respiratory disease in the adult. In the short term, we are exploring the validity of this hypothesis by accomplishing the following: (1) determining if respiratory viral infections initiate immune changes in the pulmonary microenvironment that predispose adults to pathologic responses to aeroallergens and (2) defining the molecular events initiated in response to allergen and viral insults. We believe these studies will offer intriguing new insights that will be relevant to the pathogenesis of human disease and could lead to novel interventions and/or therapy for the prevention of asthma.

Preliminary data in the laboratory demonstrated constitutive expression of several eosinophil associated ribonucleases (Ears) in the lung and the differential de novo expression of one of these Ears, Ear11, upon allergen challenge or respiratory syncytial virus (RSV) infection. The mutual activation of Ear11 by RSV and allergen suggests that Ear11 lies downstream of both processes, supporting hypotheses linking asthma immune responses and RSV infections - either as a predisposing factor or as trigger. The mechanisms involved in virus-induced asthma or asthma exacerbations are incompletely understood; however, our definition of the gene regulatory mechanism(s) controlling Ear11 expression will represent initial steps to resolve issues related to respiratory virus-induced pathologies.