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Tim Burnett

Tim Burnett

Associate Professor of Biological Sciences
Chair of Biological Sciences

Phone:

  • O 620-341-5622
  • O 620-341-5910

Education:

Ph.D. University of Kansas Medical Center, 2002
Dept.of Anatomy and Cell Biology.
B.S. University of Kansas (Cell Biology), 1997
B.S. Kansas State University (Secondary Education), 1992

Courses Taught:

Cancer Biology, MC549, Emporia State University, Emporia, KS
Graduate Seminar, GB571, Emporia State University, Emporia, KS
Cell Biology Laboratory, MC540, Emporia State University, Emporia, KS
Cell Biology, MC539, Emporia State University, Emporia, KS
Virology, MC701, Emporia State University, Emporia, KS
Pathogenic Microbiology, MC562, Emporia State University, Emporia, KS
Pathogenic Microbiology Laboratory, MC563. Emporia State University, Emporia, KS
Microbiology Laboratory , MC317 Emporia State University, Emporia, KS
General Microbiology, MC316. Emporia State University, Emporia, KS
Immunology, MC549. Emporia State University, Emporia, KS
Immunology Laboratory, MC550. Emporia State University, Emporia, KS
Frontiers in Reproduction, Marine Biological Laboratories, Woods Hole, MA.(GTA)
Cell and Tissue Biology, ATMY831, Univ.of Kansas Medical Center, Kansas City, KS (GTA)

Membership:

2003-2007 Sigma Xi, Emporia State University
2002-current American Society for Microbiology
2002-current Kansas Academy of Science
1997-2002 American Association of Immunologists
1997-2002 Sigma Xi, University of Kansas Medical Cent er

Research Interests:

My laboratory is primarily interested in the cellular and molecular mechanisms of innate immunity. Innate immunity involves various cell types and assorted immunoactive molecules whose primary function is to provide non-specific protection against a number of physiological insults. We are currently pursuing two research projects in the lab.

1) The biology of uterine natural killer cells

Natural killer (NK) cells represent a group of key effector cells in innate immunity. NK cells lyse target cells that have lost or diminished expression of MHC class I molecules, a characteristic of many tumor cells and cells infected with certain viruses. For example, the growth and metastatic spread of tumors, to a large extent, depends on their capacity to evade host immune surveillance and overcome host defenses. The critical role of these cells in the immune response to has warranted continued interest in their function. My research focuses on a subgroup of NK cells found at the maternal-fetal interface during mammalian pregnancy called uterine NK (uNK) cells. Uterine NK cells exhibit all of the hallmarks of potent cytotoxic cells, yet are merciful to the MHC class I deficient fetal placenta. The study of these cells will tell us much about the role of these cells during pregnancy and will likely provide some important understanding of the regulation of innate immunity.

2) Gut mucosal immunity

The interface between the microbe laden intestinal lumen and the body represents an interesting site for immunologists. On the one hand many of the microbes are harmless constituents that serve a useful role in the overall health of the host. On the other hand the gut mucosal epithelium represents a convenient portal of entry for food or water-borne pathogens. Careful regulation of the immune response is required to allow the growth of the former and to restrict access or limit the growth of the latter. r We are investigating the changes in gut bacterial communities and mucosal immunity in a mouse model of cystic fibrosis. We also are interested in changes that occur in the intestine as the bacterial community establishes itself immediately after birth. For this work we utilize rimary tissue culture of mouse fetal intestine and established cell culture models.

Publications

Norkina, O, T.G. Burnett and R.C. De Lisle. 2004. Bacterial overgrowth in the CFTR null mouse small intestine. Infection and Immunity 72(10): 6040-6049

Burnett, T.G ., J.S. Tash and J.S. Hunt. 2002. Investigation of the role of nitric oxide synthase 2 in pregnancy using mutant mice. Reproduction 124(1): 49-57

Burnett, T.G. and J.S. Hunt. 2000. Nitric oxide synthase-2 and expression of perforin in uterine natural killer cells. Journal of Immunology 164(10): 5243-5250

Hunt, J.S., M.G. Petroff and T.G. Burnett. 2000. Uterine leukocytes: key players in pregnancy. Seminars in Cell and Developmental Biology 11(2): 127-137

Abstracts

Snyder, C., R.C. De Lisle and T.G. Burnett. 2004. Increased bacterial load associated with the small intestine in a mouse model of cystic fibrosis. Kansas Academy of Science

De Lisle, R.C., T.G. Burnett and O. Norkina. 2004. Bacterial Overgrowth in the CFTR Null Mouse Small Intestine. Eighteenth Annual North American Cystic Fibrosis Conference.

Burnett, T.G. and J.S. Hunt. 2000. Uterine defects in NOS-2 deficient mice. FASEB J. 14(6): A1021.