Dr. Eaton is a board-certified veterinary pathologist (diplomate of the American College of Veterinary Pathologists) with research interests in bacterial pathogens of the gastrointestinal tract, host-pathogen interactions, and intestinal immunity.
Dr. Eaton has been studying H. pylori for more than 20 years and has used several animal models including germ-free piglets, gerbils, and mice to investigate a variety of bacterial colonization and virulence factors as well as aspects of host immune response. We currently use an adoptive transfer mouse model in which T cells from immunocompetent mice are adoptively transferred into H. pylori-infected immunodeficient mice. Non-transferred immunodeficient mice support large numbers of bacteria in their stomachs with no gastritis, adaptive immune response, or pathologic lesions. Mice that receive immunocompetent T cells, however, develop rapidly progressive severe gastritis. This model allows us to investigate separately the 1) direct effect of bacteria upon gastric epithelium in non-transferred mice, and 2) the effect of specific immune cells and cytokines in recipient mice.
Enterohemorrhagic E. coli (EHEC):
EHEC are Shiga-toxin producing pathogenic E. coli most often of the O157 serotype. The Eaton laboratory uses a germ-free mouse model to study bacterial factors that promote renal disease and to examine the differential expression of bacterial genes in vivo.
Germ-free and gotobiotic mice:
Dr. Eaton has established a germ-free and gnotobiotic mouse facility at the University of Michigan to derive, produce, and maintain germ-free and gnotobiotic mice for investigator use. Germ-free mice are completely free of exogenous bacterial, fungal, and viral microorganisms. They can be bred and maintained indefinitely in soft-sided bubble-type isolators, or for short periods in sterile microisolator cages in a laminar flow hood. These mice are ideal for the study of host pathogen interactions in a controlled environment, and for study of the roles of normal microbiota or their absence on host physiology and disease. Mice in our facility are currently used for the study of infectious diseases such as EHEC, Campylobacter jejuni, and Vibrio cholerae, and the role of enteric microbiota in gastric and colon cancer and host immune responses.
Liu, Z., E. S. Demitrack, T. M. Keeley, K. A. Eaton, M. El-Zaatari, J. L. Merchant, and L. C. Samuelson. 2012. IFNÎ_ contributes to the development of gastric epithelial cell metaplasia in Huntingtin interacting protein 1 related (Hip1r)-deficient mice. Lab Invest 92:1045-1057.
Eaton, K. A., J. S. Opp, B. M. Gray, I. L. Bergin, and V. B. Young. 2011. Ulcerative typhlocolitis associated with Helicobacter mastomyrinus in telomerase-deficient mice. Vet Pathol 48:713-725.
Eaton, K. A., A. Honkala, T. A. Auchtung, and R. A. Britton. 2011. Probiotic Lactobacillus reuteri Ameliorates Disease Due to Enterohemorrhagic Escherichia coli in Germfree Mice. Infect Immun 79:185-191.
Kao, J. Y., M. Zhang, M. J. Miller, J. C. Mills, B. Wang, M. Liu, K. A. Eaton, W. Zou, B. E. Berndt, T. S. Cole, T. Takeuchi, S. Y. Owyang, and J. Luther. 2010. Helicobacter pylori immune escape is mediated by dendritic cell-induced Treg skewing and Th17 suppression in mice. Gastroenterology 138:1046-1054.
Eaton, K. A., D. I. Friedman, G. J. Francis, J. S. Tyler, V. B. Young, J. Haeger, G. Abu-Ali, and T. S. Whittam. 2008. Pathogenesis of renal disease due to enterohemorrhagic Escherichia coli in germ-free mice. Infect Immun 76:30543063.