Assistant Professor of Molecular Microbiology and Immunology (Research)


My primary research interests are directed towards understanding the immunopathogenesis of lung injury and repair. Chitinase 3-like 1 (CHI3L1), which is also called YKL-40 in man and BRP-39 in the mouse, is a prototypic chitinase-like protein (CLP) that binds but does not cleave chitin. My recent publications demonstrate that CHI3L1 plays a protective role by ameliorating cell death and stimulating fibroproliferative repair. Specifically, CHI3L1 is stimulated in IPF where it represents an attempt to diminish injury and induce repair. In addition to IPF, pulmonary fibrosis is the major cause of morbidity and mortality in a subset of patients with Hermansky-Pudlak Syndrome (HPS), which comprises a group of inherited disorders caused by mutations of biogenesis of lysosome-related organelle complex-3 (BLOC-3). We demonstrate that circulating CHI3L1 levels are higher in HPS patients with pulmonary fibrosis compared to those that remain fibrosis-free, and that these levels associate with disease severity. Using murine models we also demonstrate that a defect in CHI3L1 inhibition of epithelial apoptosis and exaggerated CHI3L1-driven fibroproliferation play important roles in HPS fibrosis. Lastly we demonstrate that these divergent responses are mediated by differences in the trafficking and effector functions of two CHI3L1 receptors. My future research plans are aimed at dissecting the common mechanisms that underlie the pathogenesis of pulmonary hypertension and pulmonary fibrosis, specifically the roles of CHI3L1 and its receptors, and intracellular receptor trafficking pathways in disease progress. My long-range research goals are to identify the immune and cellular responses that mediate lung injury and repair responses and to identify specific molecular targets that can be targeted in the treatment of related disorders.

Brown Affiliations

Research Areas