Mark Looney, MD
|School||UCSF School of Medicine|
|Address||513 Parnassus Ave|
San Francisco CA 94143
|University of California, San Francisco||Residency ||2001||Internal Medicine|
|University of Tennessee||M.D.||1998||School of Medicine|
Mark R. Looney, MD is a Professor of Medicine and Laboratory Medicine and Attending Physician on the Pulmonary Consult Service and the Intensive Care Units at UCSF. He received his undergraduate degree from Lipscomb University in Nashville, Tennessee in 1994 and his medical degree from the University of Tennessee, Memphis in 1998. He then came to UCSF where he completed his residency in Internal Medicine and a fellowship in Pulmonary and Critical Care Medicine. He received his research training in the Cardiovascular Research Institute at UCSF under the direction of Dr. Michael Matthay (2003-2008) and started his own laboratory at UCSF in 2008.
My laboratory conducts research on acute lung injury (ALI) and we have focused our interests on the role of the innate immune response in producing lung endothelial and epithelial permeability. Using mouse models of ALI and two-photon intravital microscopy in the lung, we are investigating the interactions between neutrophils, platelets, and other immune cells in the lung microcirculation. Platelets are increasingly recognized as critical mediators of inflammation and injury, and we are using anti-platelet therapies as novel approaches to the prevention and treatment of ALI. We have also found that activated platelets can trigger neutrophil extracellular trap (NET) formation in the lung, and we are investigating the significance of NET formation in infectious and non-infectious models of ALI.
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 (ischemia-reperfusion injury) 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 are responsible for graft dysfunction.
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