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James B. Bliska

Publications

Center for Infectious Diseases

Recent lab photo

 

 

 
James B. Bliska

Professor

Center for Infectious Diseases
Ph.D., University of California-Berkeley, 1987

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(631) 632-8782
(631) 632-9797

   
Research

Dr. Bliska’s research seeks to understand molecular mechanisms that underlie pathogenesis or host protection during host-microbe cell interactions. In particular, he is interested in studying the activities of virulence factors that promote pathogenesis as well as trigger protective host innate and adaptive immune responses. The closely related Gram-negative bacteria Yersinia pseudotuberculosis and Yersinia pestis are used as model human pathogens to understand this dual nature of virulence factors. Y. pseudotuberculosis and Y. pestis are facultative intracellular pathogens and both use a highly conserved type III secretion system to deliver multiple effector proteins into the plasma membrane and cytoplasm of host cells. Numerous experimental approaches, including genetics, cell biology, immunology, structural biology, and functional evolutionary genomics, are used to determine how the type III secretion system and other Yersinia virulence factors work to promote disease or protective immunity. Specific questions being asked include: How do these bacteria prevent phagosome acidification and survive in macrophages? Which components of the type III secretion system are important for generating protective innate and adaptive immune responses in the host? How does the activity of one effector impact the immune response to another effector? Has allelic variation of virulence factors contributed to the process by which a bacterium with low pathogenic potential (Y. pseudotuberculosis) evolves into a bacterium with extremely high pathogenic potential (Y. pestis)?

Analysis of Yersinia pestis replication in activated macrophages by microscopy. Primary murine macrophages were infected with Y. pestis and activated with interferon gamma. De novo expression of green fluorescent protein was induced in viable intracellular Y. pestis. Images obtained by phase contrast and widefield fluorescence microscopy are shown as an overlay. Note the presence of green bacteria within spacious phagosomes. The bacteria are often found slightly elongated and apposed to the phagosomal membrane. From Pujol et al. Infect. Immun. 2009.

Department of Molecular Genetics and Microbiology
Stony Brook University
Stony Brook, New York 11794-5222
Phone: 631-632-8800
Fax: 631-632-9797

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