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Ongoing Projects

Thrombin activation and lung lymphatic thrombosis in the pathogenesis of COPD

Our recent work uncovered that LEC injury and lymphatic vessel thrombosis are early events after cigarette smoke exposure. We have also identified lung lymphatic thrombosis in human lung tissue from patients with COPD that is linked to COPD severity.

Ongoing studies in the lab use a mouse model of cigarette smoke exposure and human tissue to elucidate the role of thrombin activation and lymphatic thrombosis on the pathogenesis of COPD. Through these studies, we hope to define the manner in which lymphatic dysfunction and thrombosis define disease progression in COPD and thereby elucidate an entirely novel class of therapeutic targets based on lymphatic function.

Defining lung lymphatic endothelial cell heterogeneity and mapping the lymphatic response to injury 

Using transcriptomics, proteomics, and microscopy, we are working to elucidate the lung-specific heterogeneity of the lymphatic vasculature and map the response to lung injury in lung lymphatic endothelial cells in both mouse and human lung tissue. We are interested in determining the lymphatic endothelial subsets that define lung lymphatic function, as well as the molecular mechanisms for lymphatic dysfunction that drive lung injury.

The role of the lymphatic vasculature in modulating the lung immune milieu

Lymphatic dysfunction leads to marked changes in the lung immune milieu leading to the formation of tertiary lymphoid organs (TLOs). Because of this, lymphatic dysfunction has significant consequences on the response to lung injury. Ongoing work seeks to determine the role of the lymphatics in TLO formation, and the molecular pathways that define crosstalk between the lymphatic endothelium and the immune response to injury.

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