Christopher Schafer, PhD

During many infectious diseases, the blood vessels of the lung become destabilized and this undermines the lung's function by preventing the efficient exchange of oxygen. However, it is not clear why the lung's blood vessels are so susceptible to dysfunction. In the project, we hope to address this gap in our understanding by investigating an interesting process in which blood vessels of the lung, but no other organ, respond to bacterial and viral infections by reducing the expression of a specific protein known as ERG. ERG plays a critical role in maintaining vessels stability. Therefore we believe that the loss of ERG specifically within the lung may provide contribute to the lung's susceptibility to destabilization.

Update: Within the previous year, ALA Catalyst award funds have been instrumental in continuing my research into understanding how lung blood vessels behave during infectious diseases. I am now detailing a mechanism by which pulmonary blood vessels respond to inflammatory stimulation by repressing the expression of the transcription factor ERG. My data indicate that the loss of ERG expression results in the destabilization of lung blood vessels and that this then leads to the recruitment of immune cells into the lung. Therefore, our current hypothesis is that the loss of ERG expression in the lung plays a critical role in coordinating vascular response to inflammation.