My laboratory has a longstanding history of cellular and molecular investigations into the pathogenesis of lung injury and repair. We use murine modeling systems that were pioneered in our lab, genetically modified mice that were generated using these systems and human samples. We attempt to work in an iterative fashion, going from mouse to man and back again, to define basic paradigms of biology and their relevance to important human lung diseases. Major foci of the lab include (a) mechanism of Th2 inflammation and remodeling in the lung with a focus on asthma, (b) mechanisms of cigarette smoke-induced lung injury with a focus on COPD, (c) mechanisms and biomarkers of injury and repair in pulmonary fibrosis with a focus on IPF, Hermansky Pudlak Syndrome (HPS) and scleroderma, (d) chitinases and chitinase-like proteins (C/CLP) such as chitinase 3-like-1 (Chi3l1), chitinase 1 and acidic mammalian chitinase (AMCase) in lung injury and repair (e) the receptor systems for chitinase-like proteins, (f) the roles and regulation of chitinase 3-like-1 in primary and metastatic lung cancer, and (g) genetic modifiers of TGF-B1 and other mediators of injury and fibrosis.