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Robert Freishtat

Robert Freishtat

Professor of Pediatrics
Professor of Emergency Medicine (Secondary)

Office Phone: 202-476-2971
Email: Email
Department: Pediatrics

Education

  • BS, Pennsylvania State University, 1993
  • MPH, George Washington University, 2003

Biography

Robert J. Freishtat, MD, MPH is currently the Associate Chief for Academic Affairs in the Division of Emergency Medicine, Children's National Health System and Associate Professor of Pediatrics, Emergency Medicine, and Integrative Systems Biology, George Washington University School of Medicine and Health Sciences. He received his MD from the University of Maryland School of Medicine and residency training in Pediatrics at the University of Rochester Strong Memorial Hospital. This was followed by a clinical fellowship in Pediatric Emergency Medicine at Children’s National. During this time, he completed a MPH in Epidemiology and Biostatistics at the George Washington University School of Public Health and Health Services. He has remained on faculty at Children’s National for 12 years during which time he has served in a joint clinical and applied research role. Dr. Freishtat’s research has been continuously funded by the National Institutes of Health since 2003 including K23 and R01 grants. He is the principal investigator of The AsthMaP™ Project which serves as the foundation for an international collaborative effort he leads conducting systems biology investigations of injury/repair in the lung. This research focus has led to the discovery of a central theme in pathological tissue repair, specifically the concept of “Regenerative Asynchrony” in which asynchronous repair processes (e.g. mitotic cell cycles) result in fibrosis and chronic inflammation. He has authored or co-authored over 75 articles and book chapters in the fields of lung injury, asthma, and emergency medicine. In addition, he was a recipient of the 2011 International Klosterfrau Award for Research of Airway Diseases in Childhood. Dr. Freishtat is Past-President of the American Federation for Medical Research and an active member of the American Thoracic Society and Society for Pediatric Research. He is a member of the NHLBI Mentored Transition to Independence (MTI – K99/R00) Study Section. He is on the editorial board of the American Journal of Respiratory Cell and Molecular Biology and reviews for multiple journals.

Grants

2K12HD001399-16 (Batshaw/Teach, MPI)                           12/1/15 – 11/30/20  
NIH, NICHD                                                                       
Child Health Research Career Development Award at Children’s National
The purpose of the Child Health Research Career Development Award (CHRCDA) program at the Children's National Health System/Children's Research Institute is to facilitate the development of successful basic science and translational research careers for junior faculty members in pediatrics.
Role: Recruitment Officer
 
1R21AI 129909-01 (Hasegawa, PI)                                       9/30/15 – 9/29/17       
NIH, NIAID                                             
Cytokines & transcriptome in rhinovirus bronchiolitis and risk of incident asthma
The overall objective of this R21 application is to discover modifiable biomarkers in the airway of infants with RV bronchiolitis that predict incident asthma.
Role: Co-Investigator
 
1R01MD007075-01 (Freishtat, PI)                                        4/1/12 – 3/31/17         
NIH, NIMHD                                                                       
Vitamin D, Steroids, and Asthma in African American Youth
The overall goal of these experiments is to provide critical epidemiological/molecular information that will inform the interpretation of ongoing and impending randomized clinical trials of vitamin D supplementation in asthma, especially with regard to urban AA youth with asthma.
Role: Principal Investigator
 
MAA Winter 2015 Predoctoral Fellowship (Ferrante, PI)     7/1/15 – 6/30/17              
American Heart Association                                        
Cardiovascular Disease Risk in Obese Youth: Adipocyte Exosomal Impairment of Macrophage Cholesterol Efflux
The experiments proposed will define a mechanism by which obesity in youth can impair cholesterol efflux in macrophages and potentially lay the foundation for the pathogenesis of adult cardiovascular disease.
Role: Sponsor
 
Drug Development Grant (Freishtat, PI)                                2/1/15 – 6/30/16         
The Clark Charitable Foundation                                        
A Preclinical Model for Personalized Drug Development in Severe Therapy-Resistant Asthma
Our goal is to add substantive new data to our published data in support of a rare disease designation for severe therapy-resistant asthma from the FDA and/or EMA. This will enable orphan drug designation for future compounds to be tested in our asthma xenograft model.
Role: Principal Investigator
 
1R01GM099773 (Hector Wong, PI)                                      8/7/12 – 6/30/16        
NIH, NIGMS                                                              
Stratification of Pediatric Septic Shock
The overarching theme of this proposal is the development of clinically applicable strategies to stratify patients with septic shock. We propose that the development of robust stratification strategies for septic shock will be an effective approach to reduce and manage heterogeneity, and thus lead to the conduct of more rational clinical trials and ultimately to the design of more individualized patient management strategies, in an analogous manner to that of the oncology field.
Role: Site PI

Awards

Societies and Honors
            Society Memberships

2003 – Present            American Thoracic Society

  • Assembly on Respiratory Cell and Molecular Biology
  • Stem Cell Working Group (2012-2015)
  • Program Planning Committee (2014-2017)
  • Chair, Stem Cell Working Group (2015-2017)
  • Assembly on Pediatrics

2003 – Present            American Federation for Medical Research

  • Eastern Region Chair-Elect (2008-2009)
  • Eastern Region Chair (2009-2011)
  • National Leadership Council (2008-2016)
  • Secretary-Treasurer (2009-2012)
  • President-Elect (2012-2013)
  • President (2013-2014)
  • Chairman and Past-President (2014-2016)

2007 – Present             Society for Pediatric Research
2010 – 2016                Federation of American Societies for Experimental Biology

  • Publications & Communications Committee (2010-2014)
  • Board of Directors, Advisor (2012-2014)
  • NIH Issues Subcommittee (2013-2015)
  • Board of Directors (2014-2016)

            Honors
2004                            Henry Christian Young Investigator Award, American Federation for Medical Research
2005                            Henry Christian Young Investigator Award, American Federation for Medical Research
2005                            National Award Winner, 2nd Annual Respiratory Disease Young Investigators’ Forum
2006                            National Finalist, 3rd Annual Respiratory Disease Young Investigators’ Forum
2008                            Faculty Award for Basic and Translational Research, 8th Annual Children’s National Medical Center Research Day
2011                            International Klosterfrau Award for Research of Airway Diseases in Childhood
2013                            American Thoracic Society Pediatric Assembly’s 1st Annual Robert Mellins Endowed Outstanding Achievement Award
2014                            Children’s Research Institute Mentoring Award for Excellence in the Field of Basic and Translational Science

Research

Systems Biology of Asthma
Asthma is a chronic inflammatory disease of the lower respiratory tract characterized by airway hyperresponsiveness and mucus obstruction. Pharmacologic analogues of cortisol (e.g. prednisone) have been used clinically since 1948 and remain standard of care for the treatment of a variety of inflammatory diseases including asthma. These glucocorticoids (GC) reduce pathological inflammation that is central to asthma, and they are thought to control clinical asthma symptoms through their anti-inflammatory effects. Curiously, anti-inflammatory agents that specifically target inflammatory cells (e.g. eosinophils, T and B cells) and their intercellular signaling pathways have not shown similar efficacy to GCs in human trials. This argues against the idea that asthmatic inflammation is merely the result of interactions between external stimuli and classic inflammatory cells like eosinophils and T cells. Rather, it is likely to involve complex interactions among multiple cell types including non-inflammatory resident cells of the lung (i.e. airway epithelium, fibroblasts, and smooth muscle). In an effort to clarify this inconsistency, we recently proposed a model placing airway epithelium at the center of a network of interacting inflammatory mediators. Due to its ability to simultaneously respond to airborne pathogens and environmental challenges and interact with its tissue environments, airway epithelium is regarded as a key lung tissue in asthma. In addition, airway epithelium communication with lamina propria fibroblasts and smooth muscle has been described. Our work is directed to understanding how steroids (e.g. GCs, Vitamin D, etc.) interact to regulate regeneration and inflammation of airway epithelium in asthma. 

Drug Development for Sepsis
Despite several decades worth of advances in antimicrobials, critical care, and organ support modalities, mortality rates from sepsis have remained largely unchanged at about 40%. In fact, sepsis is responsible for 215,000 deaths annually in the US, which is akin to mortality from acute myocardial infarction, making it the 10th leading cause of death. The frequent clinical precursor to mortality from sepsis is multiple organ dysfunction syndrome (MODS). One of the organ systems to most commonly fail is immunity: Sepsis-related immunodeficiency results in part from profound lymphoid apoptosis. Indeed, end-organ apoptosis is considered a diagnostic hallmark of progressive sepsis and MODS. Importantly, platelets have been shown to accumulate in many of the commonly affected end-organs (e.g. spleen and lung) in sepsis. Platelets are anucleate cell fragments, having only cytoplasmic components imparted by megakaryocytes residing in the bone marrow, and are incapable of de novo gene transcription. For many years, platelets were thought to be essentially protein donors for thrombotic cascades. However, recent evidence supports platelet function as a pseudo-cell, with many signal transduction pathways and translation control mechanisms fully intact. Platelet biology studies have been limited by the long-standing assumption that changes in platelet function were entirely at the post-transcriptional level. However, we recently reported sepsis-induced acute alterations in the megakaryocyte-platelet transcriptional axis that resulted in a strongly lymphotoxic platelet phenotype via expression of potent serine protease granzyme B (GzmB). This finding established the foundation for a potential paradigm shift in the study of sepsis and platelet pathobiology (i.e. megakaryocytes produce platelets with an acutely altered transcriptome resulting in a new platelet phenotype). Our investigations are centered around platelet inhibition as a means for preventing MODS in sepsis.

Link to PubMed publications: http://www.ncbi.nlm.nih.gov/pubmed/?term=freishtat+rj

Publications

View publications by this faculty member from January 1, 2013 - present

Additional publications published before January 1, 2013 may be available within Himmelfarb Library's database.

Industry Relationships and Collaborations

This faculty member (or a member of their immediate family) has reported a financial interest with the health care related companies listed below. These relations have been reported to the University and, when appropriate, management plans are in place to address potential conflicts.

  • None