Innate Immunity and Matrix Interactions Regulate Lung Injury and Repair
We are interested in the role of innate immune components (Toll-like receptors) in lung injury, repair and fibrosis. We are using genetically modified mice targeting TLR receptors, TLR signaling molecules, and hyaluronan synthase to investigate the mechanism of TLR components in pulmonary fibrosis.
Molecular Mechanisms of Lung Fibrogenesis
We are interested in the sources of fibrotic fibroblasts, the role of beta-arrestins in fibrogenesis, and the transcriptional control of fibroblast activation.
Figure 3. Genetic cell lineage tracing was used to identify the sources of fibrotic fibroblasts.
Role of Chemokines and Chemokine Receptors in Lung Injury and Repair
We are studying the immunoregulatory and molecular roles of CXCL10, CXCR3, CXCL12, and CCL2 in lung injury and repair, using transgenic and knockout mice to define the mechanisms of these chemokines and their receptors in pulmonary fibrosis, especially stem cell recruitment and maintenance, inflammatory cell recruitment and activation, and epithelial cell integrity.
Role of MicroRNA Lung Injury
We are also studying the role of microRNA in lung injury and repair, by examining microRNA expression pattern during tissue injury and generating genetically modified mice targeting specific miRNAs.