Department / Division:
Medicine / Pulmonary, Allergy, and Critical Care

Address:
DUMC 3315
Durham, NC 27710

Appointment Telephone:
919-668-7630

Office Telephone:
919-684-6143

Fax Telephone:
919-684-6002

• MD, Johns Hopkins University School of Medicine (Maryland), 1975

• Medicine, Johns Hopkins Hospital (Maryland), 1975-1977
• Pulmonary and Critical Care, Duke University Medical Center, 1980-1981

Clinical Interests:
Critical care medicine, interstitial lung diseases, sarcoidosis, pulmonary alveolar proteinosis, diving and hyperbaric medicine

Research Interests:
Dr. Piantadosi's laboratory has a special expertise in mechanisms of acute organ failure, especially lung injury (ALI), and an emphasis on the molecular biology that governs the importance of the physiological gases— oxygen, carbon monoxide and nitric oxide— in the pathogenesis and regulation of the responses to acute tissue injury. The basic science focuses on the control of oxidative metabolism by redox mechanisms, and the effects of reactive oxygen and nitrogen species in acute inflammatory lung injury. Because clinically ALI has such a high mortality, which is poorly understood scientifically, the objectives of work are to elucidate mechanisms of ALI related to the activation and deregulation of host defenses and crosstalk between inflammation and coagulation by redox events produced during exposure to hyperoxia, bacterial infection, and cytokines/chemokines elaborated as part of innate immunity. The approach relies on physiology, pathology, and cell and molecular biology to measure the integrated response to injury in order to decipher the injury mechanisms as well as to design and test specific interventions to prevent them. Another portion of the work is devoted to understanding the implications of ALI in terms of failure of non-pulmonary organs, which is a key to understanding the high mortality of this patient population. The organ systems of interest include the heart, brain, liver, and kidney, and especially the tissue damage caused by sepsis and septic shock. The laboratory focuses on animal models of disease, most heavily transgenic and knockout mice, in order to understand how inflammatory pathogenesis impacts onmitochondrial energy provision, mitochondrial damage and signaling through the intrinsic programmed cell death (apoptosis) pathways as well as in organ recovery through mitochondrial biogenesis and cell proliferation.

Representative Publications:
Suliman HB, Carraway MS, Tatro LG, Piantadosi CA. A new activating role for CO in cardiac mitochondrial biogenesis. J Cell Sci. 2007 Jan 15;120(Pt 2):299-308. (2007) Abstract

Suliman HB, Carraway MS, Ali AS, Reynolds CM, Welty-Wolf KE, Piantadosi CA. The CO/HO system reverses inhibition of mitochondrial biogenesis and prevents murine doxorubicin cardiomyopathy. J Clin Invest. 2007 Dec;117(12):3730-41. (2007) Abstract

Haden DW, Suliman HB, Carraway MS, Welty-Wolf KE, Ali AS, Shitara H, Yonekawa H, Piantadosi CA. Mitochondrial biogenesis restores oxidative metabolism during Staphylococcus aureus sepsis. Am J Respir Crit Care Med. 2007 Oct 15;176(8):768-77. (2007) Abstract

Piantadosi CA, Suliman HB. Mitochondrial transcription factor A induction by redox activation of nuclear respiratory factor 1. J Biol Chem. 2006 Jan 6;281(1):324-33. (2006) Abstract

Suliman HB, Welty-Wolf KE, Carraway MS, Schwartz DA, Hollingsworth JW, Piantadosi CA. Toll-like receptor 4 mediates mitochondrial DNA damage and biogenic responses after heat-inactivated E. coli. FASEB J. 2005 Sep;19(11):1531-3. (2005) Abstract

Piantadosi CA, Schwartz DA. The acute respiratory distress syndrome. Ann Intern Med. 2004 Sep 21;141(6):460-70. (2004) Abstract

Suliman HB, Carraway MS, Welty-Wolf KE, Whorton AR, Piantadosi CA. Lipopolysaccharide stimulates mitochondrial biogenesis via activation of nuclear respiratory factor-1. J Biol Chem. 2003 Oct 17;278(42):41510-8. (2003) Abstract