Goal

Our laboratory studies mechanisms underlying normal and aberrant host response to respiratory pathogens, the molecular basis of distinct host-pathogen interactions triggering lung injury, and host factors that promote protection and resilience during lower respiratory tract infection. We utilize relevant respiratory pathogens to understand how infection leads to collateral damage that impact the function of the alveolar capillary barrier interface. Our laboratory utilizes molecular genetic approaches, in vitro biochemical assays, in vivo murine models, and bio-samples from human cohorts to address questions related to the control of inflammation in lung injury. Core strength of the lab is immune and non-immune cell phenotyping, evaluation of pulmonary host defense and respiratory mechanics in murine models, and advanced optical imaging of the lung.

Cellular and molecular events in healthy lung and during acute lung injury (ALI).
In ALI, there is disruption of the alveolar capillary barrier leading to extravasation of inflammatory cells, proteinaceous edema fluid, platelets and megakaryocytes into the interstitial space that contribute to dynamic matrix remodeling. Establishment of a provisional matrix is critical for optimal repair of the injured lung.
Immunofluorescent image of the murine lung after injury.
Immunofluorescent image of megakaryocytes (red) in alveolar interstitium from human pulmonary fibrosis lung. Lung tissue explant obtained courtesy of Dr. Derek Byers and Dr. Steve Brody.
Inflammatory cells (green) and megakaryocytes (red) in human COPD lung.
Lung tissue explant obtained courtesy of Dr. Derek Byers and Dr. Steve Brody.
Periodic acid-Schiff (PAS) staining of mouse lung tissue following infectious injury shows increase in mucin expression (magenta) along the bronchial epithelium.