Our laboratory primarily studies how the immune system contributes to the development of pulmonary hypertension. We do through primarily using animals with experimental forms of pulmonary hypertension, and then studying the cells and cytokines of the immune system. We can block or delete specific cytokines or cells to alter the immune response, and then we study how this affects the pulmonary hypertension severity and other components of the immune system.

This is an immunostain for a cytokine which may contribute to pulmonary hypertension, Chi3l1, in a mouse experimentally exposed to Schistosoma mansoni. The brown cells are positive for this cytokine. They are surrounding a blood vessel which is severely diseased.   

This is an immunostain for 2 proteins, alpha-smooth muscle actin (in green) and thrombomodulin (in red), which mark the medial and intimal layers of the blood vessel, respectively. This is of S. mansoni-exposed mouse deficient in interleukin-4. The blood vessel remains thickened: we found in this publication that only mice deficient in both interleukins 4 and 13 are protected from the pulmonary hypertension.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4642207/

This an immunostain for CD3 (pink: marks T cells) and alpha-smooth muscle actin (white: marks muscle cells) in a mouse which has dendritic cells marked in green (Zbtb46-gfp). This mouse was experimentally exposed to Schistosoma mansoni. This image was taken in collaboration with Dr. Ari Molofsky's lab at UCSF.

https://www.arimolofskylab.org/

We also study how the right side of the heart reacts to the obstruction of blood flow through the lung. This is an image of the right ventricle free wall from a mouse exposed to hypoxia, another cause of pulmonary hypertension. Capillaries are marked in green (lectin stain), proliferating cells in red (PCNA), and nuclei in blue (DAPI). 

We are developing collaborations with physician-scientists in locations where schistosomiasis is endemic, including in Brazil, Ethiopia and Zambia.