Gregory Priebe, MD

Department	Anesthesiology Infectious Diseases
Hospital Title	Senior Associate in Critical Care Medicine Associate Physician in Medicine
Academic Title	Assistant Professor of Anaesthesia (Pediatrics)
Phone	617-355-7327
Fax	617-730-0453
Email	Gregory Priebe
Location	300 Longwood Avenue Division of Critical Care Medicine, Bader 634 Boston MA 02115

Research Overview

Dr. Priebe's lab studies the pathogenesis and immunology of lung infections due to Gram-negative bacterial pathogens, particularly Pseudomonas aeruginosa and members of the Burkholderia cepacia complex. P. aeruginosa is an important cause of hospital-acquired infections in critically ill and immunocompromised patients, of corneal infections in wearers of contact lenses, and of chronic lung infections in children and adults with cystic fibrosis (CF). Bacteria in the Burkholderia cepacia complex cause chronic pneumonia and bacteremia in patients with CF and chronic granulomatous disease. A focus of my research group is on the mechanisms of protection from infection elicited by live-attenuated P. aeruginosa strains as intranasal vaccines in animal models. P. aeruginosa mutants having a deletion of the aroA gene have proven to be both highly attenuated and immunogenic. We have shown that this intranasal live-attenuated vaccine protects mice against mortality from acute P. aeruginosa pneumonia and against severe eye pathology from corneal infections. Antibody alone can protect against most corneal infections. However, for protection against pneumonia, both cellular immunity (particularly T cells) and LPS-specific antibodies are needed. We have recently shown that rapid recruitment of neutrophils to the airways by the T cell-derived cytokine IL-17 is critical for effective vaccine-induced protection. Another area of active investigation centers on evaluating our live-attenuated P. aeruginosa vaccines in transgenic CF mice, which have deficient antibody responses compared with wild-type counterparts. Ongoing studies are dissecting the mechanisms behind the suboptimal antibody response of the CF mice and testing ways to improve it. Another project in the lab examines the roles of LPS and surface polysaccharides in the virulence of bacteria in the Burkholderia cepacia complex, including B. dolosa, which has caused an outbreak in the CF population at Children's Hospital Boston. Current experiments are focusing on a Staphylococcal surface polysaccharide called poly N-acetyl-glucosamine (or PNAG) as a potential target for antibody-mediated therapies of bacteria in the Burkholderia cepacia complex.

About Gregory Priebe

Dr. Priebe joined the faculty of Children's Hospital Boston in October 2001. In July 2004, he became the Associate Program Director of the Fellowship Program in Pediatric Critical Care. He also holds the position of Associate Physician at the Channing Laboratory of Brigham and Women's Hospital, where his research lab is located.

Dr. Priebe earned his medical degree from Harvard Medical School and then went on to complete residency and chief residency in Pediatrics followed by fellowships in Pediatric Infectious Diseases and Pediatric Critical Care, all at Children's Hospital Boston. He is board-certified in Pediatric Infectious Diseases and Pediatric Critical Care.

Key Publications

• Priebe GP, Meluleni GJ, Coleman FT, Goldberg JB, and Pier GB. Protection against fatal Pseudomonas aeruginosa pneumonia in mice after nasal immunization with a live, attenuated aroA deletion mutant. Infect. Immun. 2003;71(3):1453-61.
   
• Priebe GP, Dean CR, Zaidi T, Meluleni GJ, Coleman FT, Coutinho YS, Noto MJ, Urban TA, Pier GB, Goldberg JB. The galU gene of Pseudomonas aeruginosa is required for corneal infection and efficient systemic spread following pneumonia but not for infection confined to the lung. Infect. Immun. 2004;72(7):4224-4232.
   
• Benarafa C, Priebe GP, Remold-O’Donnell E. The neutrophil serine protease inhibitor serpinb1 preserves lung defense functions in Pseudomonas aeruginosa infection. J. Exp. Med. 2007; 204:1901-1909.
   
• Priebe GP, Walsh RL, Cederroth TA, Kamei A, Coutinho-Sledge YS, Goldberg JB, Pier GB. IL-17 is a critical component of vaccine-induced protection against lung infection by LPS-heterologous strains of Pseudomonas aeruginosa. J. Immunol. 2008;181:4965-4975.