Medical College of Georgia

 Biochemistry and Molecular Biology

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Thompson Lab
(Dr. Stuart A. Thompson)

Summer 2006

From left: Kim Rathbun, Chris Thompson, Joo-Sung Kim, Stu Thompson, Jiaqi Li, Josh Fields, Sandy Dave, Willie Agee, Diana Murro, Katie Wilson, Mohana Pajaniappan

See more of the Thompson lab photos.

My laboratory studies two Gram-negative bacterial pathogens, Campylobacter jejuni and Campylobacter fetus.

Campylobacter jejuni is the leading cause of acute bacterial gastroenteritis in the U.S., infecting more than 2 million persons each year. The main reservoir for C. jejuni is poultry, and the majority of U.S. poultry flocks are colonized asymptomatically by C. jejuni. These bacteria often survive commercial processing and appear in retail meats; the majority of human infections appear to result from the consumption of contaminated chicken or turkey. C. jejuni is designated a Category B bioterrorism agent by the National Institutes of Health (NIH)  and U.S. Centers for Disease Control.
 

Because the internal temperatures of humans and birds are significantly different (37°C and 42°C, respectively), we are funded by the NIH to examine the role of growth temperature in the regulation of genes related to colonization and virulence. We investigate this problem using a combination of DNA microarrays and a state-of-the-art proteomic approach. Proteomics involves the use of 2-dimensional polyacrylamide gel electrophoresis to visualize fluorescently-labeled, temperature-regulated proteins; these are subsequently identified by  mass spectrometry. Once identified, C. jejuni mutants lacking temperature-regulated proteins can then be constructed and tested for deficiencies in virulence-related properties. These studies have also led to the identification of a novel mechanism for global gene regulation in C. jejuni.
 

Campylobacter fetus is predominantly a veterinary pathogen although it also causes severe disease in immunocompromised persons. The major virulence factor of C. fetus is a paracrystalline surface layer (S-layer), a protein “coat” which resists killing by the host immune system. 

The S-layer is composed of antigenically variable S-layer protein subunits (SLPs) that are transported to the cell surface in the absence of the N-terminal secretion signals used by the general secretory pathway. We recently discovered that SLPs instead are secreted by a type I pathway, similar to those that transport hemolysins, leukotoxins, and proteases from a number of bacterial species. The goals of our studies are: 1) to elucidate the location and structure of the C. fetus SLP secretion signal, 2) to investigate the interaction of the secretion signal with the transport apparatus and 3) to study the means by which the synthesis and secretion of SLPs are coordinated. Finally, we will pursue the potential use of C. fetus as a live bacterial vaccine vector, using chimeric SLPs as carriers for expressing heterologous antigens (e.g. HIV, influenza, tuberculosis) on the C. fetus cell surface.

Selected recent publications:

Yu, R.K. Usuki, S., Y. Nakatani, K. Taguchi, T. Fujita, S. Tanabe, I. Ustunomi, Y. -H. Gu, S. Cawthraw, D.G. Newell, M. Pajaniappan, S.A. Thompson, and T. Ariga. 2008. Topology and patch-clamp analysis of the sodium channel in relationship to the anti-lipid A antibody in campylobacteriosis, J. Neurosci. Res., in press.

Fields, J.A., and S.A. Thompson. 2008. Campylobacter jejuni CsrA mediates oxidative stress responses, biofilm formation, and host cell invasion. J. Bacteriol., 190(9):3411-3416.

Pajaniappan, M., J.E. Hall, S.A. Cawthraw, D.G. Newell, E.C. Gaynor, J.A. Fields, K.M. Rathbun, W.A. Agee, C.M. Burns, S.J. Hall, D.J. Kelly, and S.A. Thompson. 2008. A temperature-regulated Campylobacter jejuni gluconate dehydrogenase is involved in respiration-dependent energy conservation and chicken colonization. Mol. Microbiol., 68(2):474-491.

Ahmed-Barnes, I.H., M.C. Bagnall, D.D. Browning, S.A. Thompson, G. Manning, and D.G. Newell. 2007. y-glutamyl transpeptidase has a role in the persistent colonization of the avian gut by Campylobacter jejuni. Microb. Pathogen. 43(5-6):198-207.

Thompson, S.A., E.V.Maani, A.H. Lindell, C.J. King, and J.V. McArthur. 2007. Novel tetracycline resistance determinant isolated from an environmental strain of Serratia marcescens, Appl. Environ. Microbiol. 73(7):2199-2206.

Usuki, S., Pajaniappan, M., S.A. Thompson, and R.K. Yu. 2007. Chemical validation of molecular mimicry: interaction of cholera toxin with Campylobacter lipooligosaccharides, Glycocon. J. 24(2-3):167-180.

Usuki, S., S.A. Thompson, M.H. Rivner, K. Taguchi, K. Shibata, T. Ariga, and R.K. Yu. 2006. Molecular mimicry: Sensitization of Lewis rats with Campylobacter jejuni lipopolysaccharides induces formation of antibody toward GD3 ganglioside. J. Neurosci. Res. 83(2):274-284.

Tu, Z.-C., T.M. Wassenaar, S.A. Thompson, and M.J. Blaser. 2003. Structure and genotypic plasticity of the Campylobacter fetus sap locus, Mol. Microbiol. 48(3):685-698.

Thompson, S.A. 2002. Campylobacter surface layers (S-layers) and immune evasion, Annals Periodontol. 7(1):43-53.

Takata, T., E. El-Omar, M. Camorlinga, S.A. Thompson, Y. Minohara, P.B. Ernst, and M.J. Blaser. 2002. Helicobacter pylori does not require Lewis X or Lewis Y expression to colonize mice. Infect. Immun.70(6):3073-3079.

Tu, Z.-C., K.C. Ray, S.A. Thompson, and M.J. Blaser. 2001. Campylobacter fetus uses multiple loci within the 5' conserved regions of sap homologs for DNA inversion. J. Bacteriol. 183(22):6654-6661.

Ray, K.C., Z.-C. Tu, R. Grogono-Thomas, D.G. Newell, S.A. Thompson and M.J. Blaser. 2000. Campylobacter fetus sap inversion occurs in the absence of RecA function. Infect. Immun. 68(10):5663-5667.

Donahue, J., R.M. Peek, S.A. Thompson, Q. Xu, M.J. Blaser, and G.G. Miller. 2000. Analysis of iceA1 transcription in Helicobacter pylori. Helicobacter, 5(1):1-12.

Kuipers, E.J., D.A. Israel, J.G. Kusters, M.M. Gerrits, A. van der Ende, R.W.M. van der Hulst, H.P. Wirth, J. Höök-Nikanne, S.A. Thompson, and M.J. Blaser. 2000. Evidence for quasispecies development of Helicobacter pylori by study of paired isolates obtained years apart in the same host. J. Infect. Dis., 181(1):273-282.

Atherton, J.C., P.M. Sharp, T.L. Cover, G. Gonzalez-Valencia, R.M. Peek, Jr., S.A. Thompson, C.J. Hawkey, M.J. Blaser. 1999. Vacuolating cytotoxin (vacA) alleles of Helicobacter pylori comprise two geographically widespread types, m1 and m2, and have evolved through limited recombination. Curr. Microbiol. 39(4):211-218.

Thompson, S.A., O.L. Shedd, K.C. Ray, M.H. Beins, J.P. Jorgensen, and M.J. Blaser. 1998. Campylobacter fetus surface layer proteins are transported by a type I secretion system. J. Bacteriol. 180(24):6450-6458.

Achtman, M., T. Azuma, D.E. Berg, Y. Ito, G. Morelli, Z.-J. Pan, S. Suerbaum, S.A. Thompson, A. van der Ende, L.-J. van Doorn. 1999. Recombination and clonal groupings within Helicobacter pylori from different geographical regions. Mol. Microbiol. 32(3):459-470.

For more information on graduate or postdoctoral work in Microbiology in the Department of Biochemistry and Molecular Biology at the Medical College of Georgia, please contact Dr. Stuart A. Thompson.  

More information on Dr. Stuart A. Thompson, please see the MCG Institutional Faculty List or the Community of Science database

Additional Links:
Biomedical Research at MCG.
Microbiology at MCG.