Mohamed A. Elgazzar, PhD

Mohamed Elgazzar, PhD

Professor | Pulmonary Disease and Critical Care Medicine

VA Building # 1
423-439-6229

Graduate: PhD, Immunology, Kumamoto University School of Medicine, Japan, 2002
Fellowships: Department of Pediatrics, National Jewish Medical Center, Denver, CO 2003-2004; Department of Medicine, University of Colorado Health Sciences Center, Denver, CO 2004-2006; Department of Internal Medicine, Wake Forest University School of Medicine, Winston Salem, NC 2006-2007.
Special Areas of Interest: Innate immunity cell reprogramming; MicroRNAs in severe systemic inflammation; Immunopathology of chronic HIV and HCV infections.

Brief Bio

Mohamed Elgazzar, PhD, is an Immunologist and a Professor of Molecular Medicine. He received his PhD in 2002 from Kumamoto University School of Medicine, Japan. He received his postdoctoral training in Immunology at the National Jewish Medical Center and University of Colorado in Denver and in Infectious Diseases at Wake Forest University School of Medicine in Winston-Salem before joining ETSU. He holds an adjunct professor position in the Department of Biomedical Sciences. He has authored more than 84 articles in peer-reviewed journals.

As a Molecular Immunologist with broad-based training in immunology and infectious diseases, Dr. Elgazzar's research has focused on molecular processes that can be translated to the field of inflammation, with a focus on severe systemic inflammatory processes like sepsis. His specific contributions and emphasis are on epigenetic and microRNA based regulation that generates reprogramming of genes linked to inflammation. His recent work indicates that microRNAs play a role in sepsis pathogenesis, including immunosuppression and chronic inflammation, a poorly understood and highly prevalent aspect of sepsis that increases rates of mortality to infection or injury. His work is at the forefront of sepsis research, having developed a preclinical model of sepsis that can be followed over an extended period of time and that allows for manipulating the immunosuppressive state of post-acute sepsis.