- Lab: 859-218-4026
- MS 423
Undergraduate: B.S. Biochemistry and Molecular Biology, Centre College
Ph.D.: Microbiology, University of Kentucky
Postdoc: Laboratory of Intracellular Parasites, Rocky Mountain Labs, NIAID
The bacterium Chlamydia trachomatis is an agent of sexually transmitted disease and represents the number one infectious agent reportable to the U.S. Centers for Disease Control. Primary infections do not elicit long-term protective immunity, re-infections are common, and C. trachomatis has a tremendous negative impact on human reproductive health world-wide. Chlamydiae are spherical, obligate intracellular pathogens that parasitize human cells from within specialized vacuoles termed inclusions. The capacity to cause disease depends directly on the ability of chlamydiae to establish and maintain this protected intracellular niche.
The Fields lab focuses on understanding how chlamydial infections result in disease by elucidating the molecular mechanisms employed by Chlamydia spp. to subvert and evade host defenses. Effort is focused on understanding how the chlamydial type III secretion system is employed to manipulate host cell biology. We are particularly intereseted in understanding what anti-host proteins are being secreted, what host cell pathways are targeted, and how overall secretion activity is linked to the chlamydial developmental cycle.
NIH RO1AI065530. Type III exported effectors of Chlamydia trachomatis.
NIH R21AI144648. Conditional null mutants in the study of essential gene products of Chlamydia
NIH F31AI147147-01. (Gabrielle Keb). Chlamydia trachomatis Secreted Effector Proteins: Infection Properties and Identification of Host Targets.
Keb, G., Hayman, R., and K.A.Fields. 2018. Floxed-cassette allelic exchange mutagenesis enables marker-less gene deletion in Chlamydia trachomatis and reverses polar effects on down-stream genes. J. Bacteriol. JB.00479-18. doi: 10.1128/JB.00479-18.
Mueller, K.E., Wolf, K., and K.A. Fields. 2016. Gene Deletion by Fluorescence-Reported Allelic Exchange Mutagenesis (FRAEM) in Chlamydia trachomatis. mBio. e01817-15.
Ferrell, J.C. and K.A. Fields. 2015. A working model for the type III secretion mechanism in Chlamydia. Microbes Infect. Doi 10.1016/j.micinf.2015.10.006.
Mueller, K.E. and K.A. Fields. 2015. Application of β-lactamase reporter fusions as an indicator of effector protein secretion during infections with the obligate intracellular pathogen Chlamydia trachomatis. PLos ONE. 10:e0135295.
Mueller, K., Plano, G.V., and K.A. Fields 2014. New Frontiers in type III secretion biology: The Chlamydia perspective. Infect Immun. 82:2-9. PMID 24126521
Fields, K.A., McCormick, R., de Armas, L., and E.R. Podack. 2013. Perforin-2 restricts growth of C. trachomatis in macrophages. Infect Immun. 81:3045-3054. PMID23753625
Wolf, K., and K.A. Fields. 2013. Chlamydia pneumoniae impairs the innate immune response in infected epithelial cells by targeting TRAF3. J. Immunol. 190:1695-1701. PMID 23303668