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Division Chief, Division of Pulmonary, Allergy and Critical Care Medicine,
UPMC Endowed Professor and Director,
Acute Lung Injury Center of Excellence
Dr. Mallampalli received his MD from the University of Wisconsin. He completed an internship and residency in Internal Medicine at Hennepin County Medical Center in Minneapolis, MN where he also served as chief medical resident. Dr. Mallampalli completed a Pulmonary and Critical Care fellowship at the University of Iowa, where he obtained his research training under the mentorship of Dr. Gary Hunninghake. At Iowa, Dr. Mallampalli was appointed Professor of Medicine and Biochemistry and served as Associate Chair.
Dr. Mallampalli serves as Editor for the Journal of Biological Chemistry and the American Journal of Physiology. He serves on multiple peer review panels including the LIRR Study Section for NIH grant reviews. He is an elected member of the American Society of Clinical Investigation, an Established Investigator of the American Heart Association, and a Career Investigator of the American Lung Association. In September of 2009, Dr. Mallampalli was recruited as Chief of the Pulmonary Division of the VA Pittsburgh Healthcare System and as the Director of the Acute Lung Injury Center at the University of Pittsburgh.
Dr. Mallampalli’s research in the area pulmonary epithelial molecular and cell biology as it relates to acute lung injury and the mechanisms of sepsis. He is a nationally recognized investigator in the area of pulmonary lipid metabolism.
The primary goal of his research is to investigate the molecular mechanisms for control of the major phospholipid of animal membranes and of lung surfactant, phosphatidylcholine (PC). PC levels are tightly controlled, in part, by the rate-regulatory phosphoenzyme cytidylyltransferase (CCT). His work investigates the molecular physiology of how CCT is controlled by reversible phosphorylation events within its carboxyl-terminus and its regulation by enzyme turnover. In models of inflammatory lung injury, surfactant PC biosynthesis is impaired because CCT activity decreases as a result of post-translational enzyme modification and gene transcriptional repression. Specifically, he has discovered that CCT is coordinately degraded by calpains and the ubiquitin system in models of pulmonary sepsis. These adverse effects are opposed by the calcium- sensor, calmodulin, that binds and stabilizes CCT during infection. CCT is also inactivated by stress kinases stimulated during lung inflammation that target novel docking motifs and phosphorylation sites within the enzyme resulting in greatly decreased PC production.