| Name: |
| Scott D. Kobayashi |
| Title: |
| Assistant Professor |
| Degree: |
| Ph.D., 1998, Montana State University |
| Phone: |
| (208) 885-0805 |
| Fax: |
| (208) 885-6518 |
| Email: |
| sdkobi@uidaho.edu |
| Lab/Office Location: |
| Ag Biotech, Room 222 |
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| Research Interests: |
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Human polymorphonuclear leukocytes (PMNs or neutrophils) are the primary innate host defense against invading bacterial pathogens.
Neutrophils are rapidly recruited to sites of infection and ingest microorganisms through a process known as phagocytosis. Following
phagocytosis by human PMNs, microorganisms are killed by reactive oxygen species (ROS) and microbicidal products contained within
granules. The ability of PMNs to effectively remove pathogens is essential for the maintenance of human health. Although the
majority of microorganisms are readily killed by PMNs, several important bacterial pathogens have evolved the capability to subvert
the human innate immune system to cause disease. Strategies used by bacteria to circumvent innate host defense are extremely diverse
and include evasion of phagocytosis, inhibition of phagosome-lysosome fusion, and resistance to killing.
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The research focus of my laboratory is geared towards understanding the molecular basis of host-pathogen interactions, and in
specific, the innate immune response to Yersinia pestis. Y. pestis, the causative agent of plague, is one of the most
virulent and notorious of all human pathogens. Plague is responsible for three major pandemics which occurred in the 6th, 14th, and
20th centuries and resulted in approximately 100, 44, and 13 million deaths, respectively. Approximately 2,000 new cases of Y.
pestis infection are reported annually and plague has recently been classified as a re-emerging disease by the World Health
Organization. The ability of Y. pestis to cause disease is based, in part, on plasmid encoded features that enable this
bacterium to subvert the innate immune response and flourish in lymphoid tissue. However, the molecular mechanisms used by this
important human pathogen to alter PMN function are not well characterized. Thus, the broad goal of our studies is to identify key
molecular processes involved in the human polymorphonuclear leukocyte response to Yersinia pestis that underlie bacterial
pathogenesis. We propose to address in depth, the role of the neutrophil in the human innate immune response against Y.
pestis by 1) investigating the mechanisms used by Y. pestis to evade phagocytosis and killing by human PMNs; and 2)
characterization of post-phagocytosis sequelae in human neutrophils exposed to Y. pestis. We anticipate that these studies
will provide both important insight into Y. pestis pathogenesis and a better understanding of the role for the human innate
immune system in defense against plague.
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| Selected Publications: |
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Jarrett, C., Deak. E., Isherwood, K.E., Oyston, P.C., Fischer, E.R., Whitney, A.R., Kobayashi, S.D., DeLeo, F.R., and Hinnebusch, B.J. 2004 Transmission of Yersinia pestis from an infectious biofilm in the flea vector. J. Infect. Dis., 190:783-792.
Kobayashi, S.D., Voyich, J.M., Braughton, K.R., Whitney, A.R., Nauseef, W.M., Malech, H.L., and DeLeo, F.R. 2004 Gene expression profiling provides insight into the pathophysiology of chronic granulomatous disease. J. Immunol., 172:636-643.
Kobayashi, S.D., Voyich, J.M., and DeLeo, F.R. Regulation of the neutrophil-mediated inflammatory response to infection. (2003) Microbes. Infect., 5:1337-1344.
Kobayashi, S.D., Braughton, K.R., Whitney, A.R., Voyich, J.M., Schwan, T.G., Musser, J.M., and DeLeo, F.R. Bacterial pathogens modulate an apoptosis differentiation program in human neutrophils. (2003) Proc. Natl. Acad. Sci. USA, 100:10948-10953.
Kobayashi, S.D., Voyich, J.M., Braughton, K., and DeLeo, F.R. 2003 Down-regulation of pro-inflammatory capacity during apoptosis in human polymorphonuclear leukocytes. J. Immunol., 170:3357-3368.
Kobayashi, S.D., Voyich, J.M., Braughton, K. R., Somerville, G.A., Malech, H.L., Musser, J.M., and DeLeo, F.R. 2003 An apoptosis differentiation program in human polymorphonuclear leukocytes facilitates resolution of inflammation. J. Leuk. Biol. 73:315-322.
Kobayashi, S.D. and Nagiec, M.M. 2003 Ceramide/Long chain base phosphate rheostat in Saccharomyces cerevisiae. Eukaryot. Cell, 2:284-294.
Kobayashi, S.D., Voyich, J.M., Buhl, C.L., Stahl, R.M., and DeLeo, F.R. Global changes in gene expression by human polymorphonuclear leukocytes during receptor-mediated phagocytosis: cell fate is regulated at the level of gene expression. (2002) Proc. Natl. Acad. Sci. USA, 99:6901-6906.
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