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Division of Biology

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Stephanie Shames, Assistant Professor

shames

Contact information

347 Ackert Hall
(785) 532-0110
sshames@ksu.edu

Lab website: https://www.shames-lab.com/

Education

Ph.D. 2011, University of British Columbia, Microbiology & Immunology.

Area(s) of Specialization

Host-pathogen interactions, bacterial pathogenesis, cellular microbiology.

Research Focus

Intracellular bacterial pathogens are a significant cause of worldwide morbidity and mortality and uncovering aspects of their interaction with host cells is critical to combatting disease.  As an accidental pathogen of humans that naturally infects unicellular protozoa, Legionella pneumophila is an excellent tool to uncover important aspects of host-pathogen interactions.  Legionella pneumophila causes a severe inflammatory pneumonia called Legionnaires’ disease in humans, which results from inhalation of contaminated aerosols and subsequent bacterial replication within alveolar macrophages.  To replicate within phagocytic cells, L. pneumophila forms a specialized compartment termed the Legionella containing vacuole (LCV).  Intracellular bacterial replication and formation of the LCV are dependent on a Dot/Icm type IV secretion system (T4SS), which functions to translocate over 300 bacterial effector proteins directly into the host cell.  The contribution of individual effector proteins to L. pneumophila virulence is largely unknown.  Revealing the molecular mechanism of effector contribution to L. pneumophila pathogenesis is critical for furthering understanding of interactions between intracellular bacterial pathogens and their hosts.  My lab is studying how L. pneumophila Dot/Icm translocated effectors influence the normal host response to infection.  Our long term goals are to understand how effectors contribute to maintenance of host cell viability and how effectors contribute to the host immune response to infection.

Selected Publications

Ngwaga, T., Chauhan, D., and Shames, S.R. 2021. Mechanisms of effector-mediated immunity revealed by the accidental human pathogen Legionella pneumophila. Front Cell Infect Microbiol. 10: 593823.

Joseph, A.M. and Shames, S.R. 2021. Affecting the effectors: Regulation of Legionella pneumophila effector function by metaeffectors. Pathogens. 10: 108.

Gilchrist, A.K., Smolensky D., Cox, S., Perumal, R., Noronha, L.E., and Shames, S.R. 2020. High-polyphenol extracts from Sorghum bicolor attenuate replication of Legionella pneumophila within RAW 264.7 macrophages. FEMS Microbiol Lett, 367(7): fnaa053.

Joseph, A.M., Pohl, A.E, Ball, T.J., Abrams, T.G., Johnson, D.K., Geisbrecht, B.V., and Shames, S.R. 2020. The Legionella pneumophila metaeffector Lpg2505 (MesI) regulates SidI-mediated translation inhibition and novel glycosyl hydrolase activity. Infect Immun, 88(5): e00853-19

Ngwaga, T., Hydock, A.J., Ganesan, S., and Shames, S.R. 2019. Potentiation of cytokine-mediated restriction of Legionella intracellular replication by a Dot/Icm-translocated effector. Journal of Bacteriology. 201(14):e00755-18.

Shames, S.R. 2019. Screening targeted Legionella pneumophila mutant libraries in vivo using INSeq. Methods in Molecular Biology. 1921:123-144.

Shames, S.R., Liu, L., Havey, J.C., Schofield, W.B., Goodman, A.L., and Roy, C.R. 2017. Multiple Legionella pneumophila effector virulence phenotypes revealed through high-throughput analysis of targeted mutant libraries. Proceedings of the National Academy of Science USA. Nov 28: 114(48)E10445-E10454.

Arasaki, K., Mikami, Y., Shames, S.R., Inoue, H., Wakana, Y., Tagaya, M. 2017. Legionella Effector Lpg1137 shuts down ER-mitochondria communication through cleavage of Syntaxin 17. Nature Communications. 8:15406.

Tørring, T., Shames, S.R., Cho, W., Roy, C.R., Crawford, J.M. 2017. Acyl-histidines: New N-acyl amides from Legionella pneumophila. ChemBioChem. 18(7): 638-46.

Shames, S.R. and Finlay, B.B. 2012. Bacterial effector interplay: a new way to view effector function.  Trends in Microbiology.  20(5):214-219.

Shames, S.R., Croxen, M.A., Deng, W., and Finlay, B.B. 2011. The type III system-secreted effector EspZ localizes to host mitochondria and interacts with the translocase of inner mitochondrial membrane 17B. Infection and Immunity. 79(12): 4784-4790.

Shames, S.R., Bhavsar, A.P. Croxen, M.A., Law, R.J., Mak, S.H.C., Deng, W., Bidshari, R., de Hoog, C.L., Foster, L.J., and Finlay, B.B. 2011. The pathogenic Escherichia coli type III secreted protease NleC degrades the host acetyltransferase p300.  Cellular Microbiology. 13(10): 1542-1557.

Sham, H.P.†, Shames, S.R.†, Croxen, M.A., Ma, C., Chan, J., Khan, M.A., Wickham, M.E., Deng, W., Finlay, B.B., and Vallance, B.A. 2011. Attaching/effacing bacterial effector NleC suppresses epithelial inflammatory responses by inhibiting NF-kB and p38-MAP Kinase activation.  Infection and Immunity. 79(9): 3552-3562 † - co-first authors.

Shames, S.R. and Finlay, B.B. 2011. Proteolytic Cleavage of NF-κB p65: A Novel Mechanism for Subversion of Innate Immune Signaling by Pathogenic E. Coli. Frontiers in Microbiology. 2 doi: 10.3389/fmicb.2011.00038.

Shames, S.R., Deng, W., Guttman, J.A., de Hoog, C.L., Li, Y., Hardwidge, P.R., Sham, H.P., Vallance, B.A., Foster, L.J., and Finlay, B.B. 2010. The pathogenic E. coli type III effector EspZ interacts with host CD98 and facilitates host cell prosurvival signaling. Cellular Microbiology. 12(9): 1322-1339.

View the complete publication list in NCBI