Research Areas

We are studying differences in the immune response to SARS-CoV-2 that may determine those that have varying degrees of outcomes both acutely and in the post-acute period.

We are testing the hypothesis that antibiotic treatment during influenza infection causes gut dysbiosis that can affect lung immunity and increase the susceptibility to post-influenza MRSA infection.

We are studying fundamental mechanisms by which syndecan-1 moderates lung inflammation after influenza infection. This research is determining how syndecan-1 regulates the airway epithelial response to influenza infection and limits lung injury through moderation of apoptosis.

We have found that syndecan-1 is upregulated by the epithelium in patients with idiopathic pulmonary fibrosis (IPF) and is a pro-fibrotic signal. Our work identified that syndecan-1 controls antifibrotic microRNA loading into extracellular vesicle in mediating this effect.

This study is a multicenter collaboration with the Bamshad group at the University of Washington and the Schroer group at Johns Hopkins University. The Bamshad group identified two coding missense polymorphisms in dynactin 4 that are highly associated with pseudomonas colonization in cystic fibrosis patients. Working with Trina Schroer, who has studied dynactin for over 15 years, we are using samples from the Bamshad patient cohort as well as cell lines to understand how these polymorphisms regulate the lung innate immune response to pseudomonas infection.