Peter Mancuso

Peter Mancuso, Ph.D.

Associate Professor, Department of Nutritional Sciences, School of Public Health
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Peter Mancuso holds an appointment in the Department of Nutritional Sciences where he teaches courses on the Pathophysiology of Obesity, Physical Activity and Nutrition, and Nutrition and the Immune Response at the School of Public Health. He is a member of the American Association of Immunologists, the American Thoracic Society, and the American Physiological Society. He received his PhD in Physiology at the University of Tennessee and completed a Post-doctoral fellowship in Pulmonary and Critical Care Medicine at the University of Michigan. His research has focused on lipid mediators, leptin receptor signaling, adipokines, and most recently, leukocyte metabolism in the host defense against bacterial pneumonia.

Research Interests

Dr. Mancuso's research falls into three different areas:1) the mechanisms by which obesity and diabetes may alter the immune response against pathogens of the lung; and 2) the role of cholesterol 25-hydroxylase in bacterial pneumonia; and 3) the role of leptin receptor signaling and other adipokines in inflammation.

  1. The prevalence of obesity has risen dramatically during the past 40 years leading to dramatic increases in chronic diseases associated with a chronic state of low grade inflammation. While obesity is a well recognized risk factor for diabetes and cardiometabolic disease, its role in infectious disease is poorly understood. Metabolic alterations that occur with obesity disrupt innate immune responses to pathogens in the lung. We are currently exploring the mechanisms by which obesity and diabetes alter metabolism and suppress bactericidal functions of alveolar macrophages and neutrophils during the course of bacterial pneumonia.
  2. The enzyme, cholesterol 25-hydroxylase (CH25H), hydroxylates cholesterol at the 25-carbon position forming the oxysterol 25-hydroxycholesterol (25-HC) which can be future metabolized to 7alpha, 25-diHC. The biological effects of 25-HC are mediated through nuclear receptors while lymphocytes express a receptor at the plasma membrane for 7alpha, 25-diHC. 25-HC plays an important role in macrophage phagocytosis of bacteria, in the regulation of IL-1beta-mediated pyroptosis, and type I IFN production during viral infections. 7alpha, 25-diHC plays a critical role in infections of the gut by regulating the accumulation and function of innate lymphoid cells and in immunity against enteric bacterial infections. We have observed that Ch25h knockout mice exhibit impaired pulmonary host defense against Klebsiella pneumonia and are currently exploring the mechanisms by which CH25H protects the lung in gram-negative pneumonia.
  3.  Leptin is best known for its role in regulating appetite and satiety. We have demonstrated that it plays an essential role in the host defense against bacterial pneumonia by activating distinct intracellular signaling pathways leading to enhanced innate immune responses in alveolar macrophages. Leptin receptor mutations have been identified in humans that contribute to impaired host defense against infections of the gut. Whether similar leptin receptor mutations play a role in susceptibility to pulmonary infections remains to be evaluated.