Department of Medicine

University of Pittsburgh

Division of Pulmonary, Allergy, and Critical Care Medicine
3459 Fifth Avenue,
628 NW
Pittsburgh, PA 15213
Academic Office: (412) 692-2210
Comprehensive Lung Center (Patient Care and Referral): (412) 648-6161

Bryan J. McVerry, MD

Assistant Professor of Medicine and Environmental and Occupational Health
Medical Director, Intensive Care Unit
Director, Translational Research in Acute Lung Injury
Director, Fellowship Program

UPMC Montefiore Hospital - NW628
3459 Fifth Avenue
Pittsburgh, PA 15213
Phone: 412-624-8735
Fax: 412-648-5980
Assistant: Stacie Truszkowski
Assistant Email:


Bryan McVerry received his B.S. in Mechanical Engineering from Lehigh University in 1992 followed by his M.D. from Georgetown University School of Medicine in 1997.  Following internship in Internal Medicine and Pediatrics, he completed residency in Internal Medicine at the University of Chicago and then went on to study out of hospital cardiac arrest during a one-year research fellowship in the Emergency Resuscitation Research Center at the University of Chicago.  He subsequently completed clinical and research fellowships in Pulmonary and Critical Care Medicine at Johns Hopkins University under the mentorship of Joe G.N. Garcia and Brett A. Simon.  In August of 2005, Dr. McVerry joined the faculty of the Division of Pulmonary, Allergy, and Critical Care Medicine at the University of Pittsburgh as Assistant Professor.  He currently serves as the Associate Director of the Medical ICU at UPMC Presbyterian Hospital, the Director of Translational Research for the Acute Lung Injury Center of Excellence, and the Associate Program Director for the Fellowship Training Program in Pulmonary and Critical Care Medicine.

Clinical Interests

Dr. McVerry’s clinical interest and expertise focuses on the care of critically ill patients in the medical ICU, specifically those with acute lung injury and ARDS.   He has additional interest in early implementation of physical rehabilitation in critically ill patients, in minimizing sedation to facilitate physical rehabilitation in mechanically ventilated patients, in endocrine dysregulation in critical illness, and in quality improvement in the Medical ICU.

Academic and Research Interests

Dr. McVerry’s research interest is focused on basic and translational investigation of the biological mechanisms underlying the development and consequences of sepsis and acute lung injury.  His research efforts are designed to span the continuum from the bench to the bedside. 

Acute lung injury (ALI) is characterized by endothelial permeability and subsequent leakage of protein and fluid into the extravascular compartment and alveoli.  Dr. McVerry’s initial work applied basic discoveries from the Garcia laboratory and demonstrated the protective effects of the endothelial barrier enhancing agent sphingosine 1-phosphate (S1P) in a translationally relevant canine model of inflammatory ALI using quantitative CT analysis to characterize regional lung edema accumulation after intratracheal endotoxin administration (McVerry et al Amer J Resp Crit Care Med 2004, Szczepaniak et al Transl Res 2008).  Endothelial dysfunction in ALI is not limited solely to the dysregulation of barrier function.  Disruption of the control of vasomotor tone in the acutely injured lung may have profound effects on regional edema formation as well as ventilation and perfusion matching and gas exchange.  In addition to its barrier protective properties, S1P has been demonstrated to modulate pulmonary vascular tone in vivo (Szczepaniak et al Amer J Physiol Lung Cell Mol Physiol 2010).  Dr. McVerry’s subsequent work in this area, supported by the American Heart Association, explores the role of endothelial nitric oxide synthase uncoupling and its production of superoxide in lieu of nitric oxide on the regulation of vascular tone and endothelial barrier integrity in the injured lung. 

Collaborative research efforts with Christopher O’Donnell, Ph.D. explore the mechanisms by which nutritional support in the setting of critical illness contributes to the development of metabolic dysfunction.  The combination of the systemic inflammatory response and caloric supplementation leads to profound peripheral insulin resistance and pancreatic dysfunction which synergize to result in dramatic glucose intolerance and hyperglycemia.  This cycle of dysfunction is associated with activation of the inflammasome and elevation in Interleukin-1β.  Ongoing work in the laboratory is focused on elucidating the mechanisms underlying metabolic dysfunction and identification of novel therapeutic targets to improve glucose utilization in sepsis. 

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Additional efforts synergize with Rama Mallampalli, MD in the Acute Lung Injury Center of Excellence to provide translational support for cutting edge bench top investigations examining novel mediators of systemic inflammation in sepsis and acute lung injury (Ray et al Nature Med 2010, Chen et al Nature Immunol 2013).  These efforts have been rewarded with program project support as well as additional NIH support through the R01 mechanism.

Key Publications

Ray NB, Durairaj L, Chen BB, McVerry BJ, Ryan AJ, Donahoe M, O'Donnell CP, Henderson FC, Etscheidt CA, McCoy DM, Agassandian M, Hayes-Rowan E, Coon TA, Butler PL, Gakhar L, Mathur SN, Sieren JC, Tyurina YY, Kagan VE, McLennan G, Mallampalli RK. Dynamic regulation of cardiolipin by the lipid pump Atp8b1 determines the severity of lung injury in experimental pneumonia. Nat Med. 2010 Oct;16(10):1120-7.

Chen BB, Coon TA, Glasser JR, McVerry BJ, Zhao J, Zhao Y, Zou C, Ellis B, Zhang Y, Mallampalli RK. A combinatorial F box protein directed pathway controls TRAF stability to regulate inflammation. Nat Immunol. 2013 May;14(5):470-9.

Watanabe Y, Singamsetty S, Zou B, Guo L, Stefanovski D, Alonso LC, Garcia-Ocana A, O’Donnell CP, McVerry BJ. Exogenous glucose administration impairs glucose tolerance and pancreatic insulin secretion during acute sepsis in non-diabetic mice. PLoS One. 2013 Jun 24;8(6):e67716.

Szczepaniak WS, Pitt BR, McVerry BJ. S1P2 receptor-dependent Rho-kinase activation mediates vasoconstriction in the murine pulmonary circulation induced by sphingosine 1-phosphate. Am J Physiol Lung Cell Mol Physiol. 2010 Jul;299(1):L137-45.

McVerry BJ, Peng X, Hassoun PM, Sammani S, Simon BA, Garcia JG.  Sphingosine 1-phosphate reduces vascular leak in murine and canine models of acute lung injury. Am J Respir Crit Care Med. 2004 Nov 1;170(9):987-93. 

PubMed Link