Peter Mancuso, PhD

Peter Mancuso is an interdisciplinary scientist whose research focuses on adipocyte derived hormones, eicosanoids, and environmental exposures that regulate pulmonary innate immune responses. He has used cellular, molecular and integrative biology to assess the effects of the eicosanoids (prostaglandins and leukotrienes), obesity, malnutrition, and tobacco smoke exposure on alveolar macrophage biology and pulmonary responses to bacterial infection. He also participates in the Graduate Program in Immunology. He is a member of the American Association of Immunologists and the American Thoracic Society. Previous to his academic appointments, he was employed as a food scientist in research and development in the food industry.

• NUTR639: Pathophysiology of Obesity
• NUTR651 Physical Activity and Nutrition
• NUTR688 Research Topics in Nutritional Sciences
• NUTR697 Readings in Nutritional Sciences
• NUTR698 Research in Nutritional Sciences
• NUTR699 Masters Thesis in Nutritional Sciences
• NUTR796 Special Topics in Nutritional Sciences

• PhD, Physiology, University of Tennessee, 1996

• M.S., Food Science and Nutrition, University of Tennessee, 1987

• B.S., Food Science, Purdue University, 1985

• Post-Doctoral Fellowship, , University of Michigan Medical Center, Lung Cell and Molecular Biology, 1997-1999

• Malnutrition is arguably the most common cause of immune suppression, from a global perspective, and a significant risk factor for infectious disease. The mechanisms responsible for impaired innate immune responses against bacterial infections arising from energy malnutrition are poorly understood. Leptin is a hormone produced by adipose tissue that is reduced in the energy malnourished and is known to regulate innate immune responses. We have observed that mice rendered leptin-deficient by genetic means or by fasting are more susceptible to bacterial pneumonia. We are currently exploring the intracellular signaling pathways by which leptin regulates alveolar macrophage function, proinflammatory mediator synthesis, and pulmonary host defense against bacterial pathogens. In addition to malnutrition, tobacco smoke is also a potent immune suppressant and smokers are very susceptible to bacterial pneumonia. Previous studies have demonstrated that pulmonary bacterial clearance and alveolar macrophage antibacterial functions are reduced in smokers. However, the mechanisms responsible for these defects are poorly understood. We are currently exploring the role of nicotine in cigarette smoke induced suppression of pulmonary innate immune responses against bacterial pathogens.

• Regulation of Pulmonary Host Defense by Leptin
  Sponsor: NIH
  
  

• Use of LTB4 as a Therapeutic Agent for the Treatment of Pneumococcal Pneumonia
  Sponsor: Adventis Pharma
  
  

• Obesity, Adipokines and Cardiovascular Risk Factors in Women
  Sponsor: NIH
  
  

• Obesity Subtypes, Adiponectin and Incident Stroke among Postmenopausal Women
  Sponsor: NIH
  
  

• Mancuso P, O Brien E, Prano J, Goel D, Aronoff DM. (2014). No Impairment in Host Defense against Streptococcus pneumoniae in Obese CPEfat/fat Mice. PLoS One e106420.

• E. O'Brien, D. Dolinoy, P. Mancuso. (2014). Bisphenol A at Levels Relevant to Human Exposure Enhances Histamine and Cysteinyl-Leukotriene Release from Bone Marrow-derived Mast Cells. Journal of Immunotoxicology 84-89.

• E.O'Brien, D.C. Dolinoy, and P.Mancuso. (January, 2014). In Utero and early-life Bisphenol A exposures increases pro-inflammatory mediator synthesis in bone marrow-derived mast cells. Journal of Immunotoxicology 205-212.

• O'Brien E, Bergin IJ, Dolinoy DC, Zaslona Z, Little RJ, Tao Y, Peters-Golden M, Mancuso P. (April, 2014). Perinatal Bisphenol A Exposure Enhances Allergen Sensitization, but Not Pulmonary Inflammation, in Adult Mice. Journal of Developmental Origins of Health and Disease 121-131.

• Peter Mancuso (August, 2012). Obesity and respiratory infections: Does adiposity weigh down host defense? Pulmonary Pharmacology and Therapeutics 412-419.

• D.M. Aronoff, I.L. Bergin, C. Lewis, D. Goel, E. O'Brien, C.H. Serezani, M. Peters-Golden, and P. Mancuso (May, 2012). Prostaglandin E2 Signaling via the E Prostanoid 2 Receptor Suppresses Pulmonary Innate Immune Defense against Streptococcus pneumoniae. Prostaglandins and other lipid mediators 23-30.

• P. Mancuso, M.G. Myers Jr., D. Goel, C.H.C. Serenzani, E. O'Brien, D.M. Aronoff, and M. Peters-Golden. (July, 2012). Ablation of leptin receptor mediated extracellular regulated kinase activation impairs host defense against bacterial pneumonia. Journal of Immunology 867-75.