Mark R. Looney, MD

My laboratory conducts research on acute lung injury (ALI), which is a syndrome produced by multiple causes including pneumonia, sepsis, trauma, and the transfusion of blood products.  ALI is responsible for 75,000 deaths in the U.S. each year and yet there is no effective pharmacotherapy to treat these patients.  We are focused on the mechanisms responsible for lung endothelial permeability, which is the hallmark of ALI. 

We have centered our interests on the role of platelets in lung inflammation and injury.  Platelets are increasingly recognized as active participants in inflammatory diseases and part of the coordinated innate immune response.  We have developed a mouse model of transfusion-related acute lung injury (TRALI) and discovered that this model is both platelet and neutrophil-dependent. We are exploring how platelets are mediating injury in TRALI and other in vivo models of ALI (LPS, acid-induced, ischemia-reperfusion) including the role of neutrophil extracellular traps (NETs).

In conjunction with the Krummel laboratory at UCSF, we have also developed a method to image the lung microcirculation using two-photon intravital microscopy.  Using a variety of transgenic fluorescent mouse strains, we are defining the migration and interactions of immune cells and platelets in the lung under normal and injury conditions.    

Finally, we are one of the few centers in the U.S. to establish a mouse lung transplantation model that we are using to study mechanisms of both early graft dysfunction (similar to ALI) and late graft dysfunction (obliterative bronchiolitis).  Lung transplantation has one of the lowest median survivals among all solid organ transplantations and we are dedicated to defining the lung-specific alloimmune responses that mediate rejection.