Pulmonary and Critical Care Medicine, acute lung injury, acute respiratory distress syndrome, blood transfusions, transfusion-related acute lung injury, neutrophils, neutrophil extracellular traps, platelets, lung transplantation
My laboratory is broadly interesting in study innate immune biology in the normal and injured lung. Using pre-clinical models of acute lung injury, we have focused on neutrophils and platelets, the latter being a bon a fide immune cell with powerful inflammatory potential. One consequence of platelet-neutrophil interactions is the formation of neutrophil extracellular traps (NETs), which we study in both sterile and pathogen-induced lung injury models. We are determining the mechanisms by which platelets trigger NETs and novel pathways to target NETs—which we have discovered are overall barrier disruptive in the lung.
We also use two-photon intravital lung microscopy as a tool for discovery. Using this technique, we have determined that the lung is a major source of mature platelet production in mice. Furthermore, megakaryocytes reside in the extravascular lung and may have potent local immune effects. The lung also contains a wide-range of hematopoietic progenitors, which have the capacity to leave the lung and engraft in the bone marrow for multi-lineage blood production. We are determining the niche-promoting factors responsible for hematopoietic progenitor residence in the lung and the contributions of these cells to the local immune repertoire.
We have an expanding interest in lung transplantation studies, including ischemia-reperfusion injury (primary graft dysfunction) and modeling chronic lung allograft dysfunction (bronchiolitis obliterans). We use the mouse single lung transplantation technique for these studies and to create lung chimeras for investigation.
UCSF Profiles Page: http://profiles.ucsf.edu/mark.looney