James B Bliska, BS, PhD
Title(s)
Professor of Microbiology and Immunology
Additional Titles/Positions/Affiliations
Distinguished Professor and Senior Lead Faculty Member of the Personalized Treatments for Cystic Fibrosis (CF) Cluster
Department(s)
Microbiology and Immunology
Education
BS, 5/83, Bacteriology, University of Wisconsin-Madison
PhD, 2/88, Molecular Biology, University of California-Berkeley
Postdoctoral, 1/93, Stanford University
Programs
Molecular and Cellular Biology Graduate Programs
Molecular Pathogenesis Program
Contact Information
Room 524A
Remsen Building
66 College Street
Hanover NH 03755
Email: James.Bliska@Dartmouth.edu
Professional Interests
RESEARCH
The focus of my research is to understand how bacterial effectors interact with the host leukocytes to trigger pathogenesis or host protection.
As a postdoc in the laboratory of Stanley Falkow, I carried out pioneering studies on a protein secretion system, now designated "type III", that is used by numerous Gram-negative bacteria to inject "effectors" into infected host cells. I collaborated with Jack Dixon and was the first to demonstrate that a type III effector could enter the host cell to act on a target protein during bacterial infection (Bliska, J. B., Guan, K., Dixon, J. E., and Falkow, S. PNAS, 1991).
As a faculty member at Stony Brook University, I continued to characterize effectors in the bacterial pathogen Yersinia and uncovered basic principles of how this class of proteins function to counteract innate immunity. Research in my laboratory also lead to the discovery that effectors can activate immune responses, providing novel insights into the immunology of infection.
The above studies culminated in my discovery of a complex interplay between three Yersinia effectors and a host protein call pyrin inside infected leukocytes (Chung et al. Cell Host Microbe, 2016). One significant outcome of this work is that it helped establish the concept of pyrin as a unique immune sensor that "guards" host cells against attack by a specific class of bacterial effectors and toxins. My current research on this project is focused on gaining a deeper understanding the Yersinia effector-pyrin interaction at the molecular and immunological levels.
In January of 2018 I joined the Department of Microbiology and Immunology at the Geisel School of Medicine as the Senior Lead Faculty Member of the Dartmouth Personalized Treatments for Cystic Fibrosis (CF) Cluster. CF is a genetic disease that results in susceptibility to lung infections by bacterial pathogens such as Pseudomonas and Burkholderia . I have initiated projects to understand how effectors secreted into leukocytes by a type III system in Pseudomonas and a type VI system in Burkholderia contribute to lung infections in people with CF. I am also exploring the use of synthetic immunology to combat bacterial lung infections in people with CF.
LEADERSHIP
As the Senior Lead Faculty Member of the Dartmouth Personalized Treatments for Cystic Fibrosis Cluster (CF Cluster), I developed a vision for its mission which is to significantly strengthen and expand the excellent translational research and training in CF and other lung diseases at Dartmouth. Benjamin Ross and Jen Bomberger were hired to complete the membership of the CF Cluster. The ongoing goals of the CF Cluster are to enhance the outstanding scientific environment, collaborative atmosphere, and cutting-edge core facilities for studies of host-pathogen interactions in the lung at Dartmouth.
Mentoring Information
I have a strong commitment to research training and career development of young scientists from diverse backgrounds at the undergraduate, graduate and post-graduate levels. I have mentored 15 graduate students, 12 to completion of the PhD and 3 remain in training. In addition, I have mentored 7 postdoctoral fellows, several of whom have obtained academic faculty positions. I am committed to increasing the diversity of individuals pursuing research-related careers. I have also been active in directing and teaching graduate level courses on topics such as CF, microbiology, molecular biology, genetics, cell biology and immunology.
Biography
1/80-8/83 Undergraduate research with Dr. Oliver Smithies
Laboratory of Genetics, University of Wisconsin-Madison
3/84-2/88 Doctoral research with Dr. Nicholas R. Cozzarelli
Department of Molecular Biology, University of California-Berkeley
3/88-1/93 Postdoctoral research with Dr. Stanley Falkow
Department of Microbiology and Immunology, Stanford University
2/93-1/99 Assistant Professor
Department of Molecular Genetics and Microbiology, Stony Brook University
2/99-4/03 Associate Professor
Department of Molecular Genetics and Microbiology, Stony Brook University
5/03-2/18 Professor
Department of Molecular Genetics and Microbiology, Stony Brook University
1/16-2/18 Director
Center for Infectious Diseases, Stony Brook University
3/18-present Professor Emeritus
Department of Molecular Genetics and Microbiology, Stony Brook University
1/18-present Distinguished Professor
Senior Lead Faculty Member of the Dartmouth Personalized Treatments for Cystic Fibrosis (CF) Cluster
Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth
Guards and decoys: RIPoptosome and inflammasome pathway regulators of bacterial effector-triggered immunity. A type VI secretion system in Burkholderia species cenocepacia and orbicola triggers distinct macrophage death pathways independent of the pyrin inflammasome. A Type VI Secretion System in Burkholderia Species cenocepacia and orbicola Triggers Distinct Macrophage Death Pathways Independent of the Pyrin Inflammasome. ExoS Effector in Pseudomonas aeruginosa Hyperactive Type III Secretion System Mutant Promotes Enhanced Plasma Membrane Rupture in Neutrophils. Phosphoprotein phosphatase activity positively regulates oligomeric pyrin to trigger inflammasome assembly in phagocytes. Neutrophil inflammasomes sense the subcellular delivery route of translocated bacterial effectors and toxins. Correction: γδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans. Role of the Yersinia pseudotuberculosis Virulence Plasmid in Pathogen-Phagocyte Interactions in Mesenteric Lymph Nodes. γδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans. The Burkholderia cenocepacia Type VI Secretion System Effector TecA Is a Virulence Factor in Mouse Models of Lung Infection. |