Dr. Priebe’s laboratory studies immunity to the bacterial pathogens Pseudomonas aeruginosa and the Burkholderia cepacia complex, with the long-term goal of developing vaccines and immunotherapies. Techniques used in his group span multiple fields, including microbiology, molecular biology, genomics, cellular and molecular immunology, and animal models of infection.
A major focus of Dr. Priebe’s lab centers on evaluation of the mechanisms of protection of live-attenuated Pseudomonas vaccines. His group showed that Pseudomonas aroA deletion mutants, given intranasally, protect mice against acute Pseudomonas pneumonia and also against corneal infections. Antibodies alone can protect against corneal infections. However, for protection against pneumonia, both T cells and LPS-specific antibodies are needed. Rapid recruitment of neutrophils to the airways by the cytokine IL-17, which is secreted by helper CD4 T cells called Th17 cells, is critical for vaccine-induced protection in the non-neutropenic host, while CD4 T cells secreting GM-CSF are needed in the neutropenic host. Dr. Priebe’s lab also recently discovered Th17-stimulating Pseudomonas protein antigens that are effective intranasal vaccines in mice. Ongoing work is aimed at improving the potency and broadness of protection of these novel vaccines.
Another project in Dr. Priebe’s lab examines the roles of LPS and surface polysaccharides in the virulence of bacteria in the Burkholderia cepacia complex (BCC), including B. dolosa, which has caused an outbreak in the cystic fibrosis population at Boston Children's Hospital. Dr. Priebe’s group showed that a staphylococcal surface polysaccharide called poly N-acetyl-glucosamine is expressed by the BCC and is a target for antibody-mediated therapies, most notably for the nearly pan-resistant B. dolosa. In collaboration with the HMS Department of Systems Biology, Dr. Priebe’s team used whole-genome sequencing of B. dolosa isolates from the Boston Children’s Hospital outbreak to identifybacterial genes under strong positive selection, suggesting potential new antibiotic targets.
About Gregory Priebe
Dr. Priebe is a Senior Associate in the Division of Critical Care Medicine of the Department of Anesthesiology, Perioperative and Pain Medicine at Boston Children’s Hospital, where he attends in the Medical-Surgical Intensive Care Unit. He is also an Associate in the Division of Infectious Diseases of the Department of Medicine at Boston Children’s Hospital and an Assistant Professor of Anaesthesia (Pediatrics) at Harvard Medical School.
Dr. Priebe serves as the Associate Program Director for the Fellowship in Pediatric Critical Care Medicine, where he is the Director of Fellowship Research. In addition to his clinical and teaching responsibilities, Dr. Priebe chairs the hospital’s Nosocomial Infection Oversight Committee, which oversees healthcare-associated infection surveillance and infection prevention practices for the hospital’s 4 ICUs. He is also active in national working groups aimed at reducing and better defining healthcare-associated infections in children.
Dr. Priebe earned his medical degree from Harvard Medical School and then went on to complete residency and chief residency in Pediatrics at Boston Children’s Hospital followed by fellowships in Pediatric Infectious Diseases and Pediatric Critical Care Medicine, also at Boston Children’s Hospital. He is board certified in Pediatric Infectious Diseases and Pediatric Critical Care Medicine.
- LiebermanTD, MichelJB, Aingaran M, Potter-Bynoe G, Roux D, Davis MR, Skurnik D, Leiby N, LiPuma JJ, Goldberg JB, McAdam AJ, Priebe GP, Kishony R. Parallel bacterial evolution within multiple patients ties novel genes to pathogenesis. Nat Genetics 2011; 43(12):1275-80(PMCID3245322).
- Skurnik D, Davis Jr. MR, Benedetti D, Moravec KL, Cywes-Bentley C, Roux D, Traficante DC, Walsh RL, Maira-Litràn T, Cassidy SB, Hermos CR, Martin TR, ThakkallapalliEL, Vargas SO, McAdam AJ, Lieberman TD, Kishony R, LiPuma JJ, Pier GB, Goldberg JB, Priebe GP. Targeting pan-resistant bacteria with antibodies to a broadly conserved surface polysaccharide expressed during infection. J Infect Dis 2012; 205(11):1709-18. Epub 2012 Mar 23 (PMCID3415848).
- Wu W, Huang J, Duan B, Traficante DC, Hong H, Risech M, Lory S, Priebe GP. Th17-stimulating protein vaccines confer protection against Pseudomonas aeruginosa pneumonia. Am J Respir Crit Care Med 2012;186(5):420-7. Epub 2012 Jun 21
- Kamei A, Wu W, Traficante DC, Koh AY, Van RooijenN, Pier GB, Priebe GP.Collaboration between macrophages and vaccine-induced CD4 T cells confers protection against lethal Pseudomonas aeruginosa pneumonia during neutropenia. J Infect Dis 2012, Epub 2012 Nov 21.
- Hong H, Morrow DF, Sandora TJ, Priebe GP. Disinfection of needleless connectors with chlorhexidine-alcohol provides long-lasting residual disinfectant activity. Am J Infect Control 2012, in press.