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Casey Theriot, Ph.D.

Description of Research: Casey Theriot

My research focuses on defining the gastrointestinal tract microbiome and metabolome during different disease states to understand how perturbations to this system affect human health. Colonization resistance describes the ability of the gastrointestinal tract to prevent colonization by pathogens. Currently, I am exploring the interactions between the gut microbiota and the pathogen Clostridium difficile, a significant and re-emerging public health problem. C. difficile infection (CDI) is the leading nosocomial infection in the United States and is becoming more commonplace in Europe. A major goal of my work is to create an integrated model of the complex interactions among the gut microbiota, pathogen and host. To accomplish this we integrate data obtained from high-throughput methods that analyze the gut microbiome, metabolome and host immune responses in mouse models and human biological specimens. It will be critically important to employ a systems biology approach to defining alterations in the gastrointestinal tract following antibiotic exposure.

My long-term research interests have always included studying infectious diseases and how they impact human health. With the advent of “omics” technologies complex communities, including the gastrointestinal tract, can be defined. A major goal of my research will be to define how metabolism of nutrients by members of the indigenous gut microbiota alters colonization resistance to C. difficile and other pathogens. Alterations in the gut microbiota have been associated with many disease states including diabetes, obesity, irritable bowel disease and other metabolic disorders. Defining the role that bacteria play in the gut will allow us to design targeted approaches for prevention and treatment of these gastrointestinal disorders.


Recent Publications:

Theriot, C.M., M.J. Koenigsknecht, P.E. Carlson, G.E. Hatton, A.M. Nelson, B. Li, G. Huffnagle, J. Li, V.B. Young. (2014) Antibiotic-induced shifts in the mouse gut microbiome and metabolome increase susceptibility to Clostridium difficile infection. Nat. Commun.5:3114 doi: 10.1038/ncomms4114.

Theriot, C.M., V.B. Young. (2014) Microbial and Metabolic Interactions between the Gastrointestinal Tract and Clostridium difficile Infection. Gut Microbes. 5(1).

Taveirne, M.E., C.M. Theriot, J. Livney, V. DiRita. (2013) The complete Campylobacter jejuni transcriptome during colonization of a natural host determined by RNAseq. PLoS One. Aug 21;8(8):e73586.

Sadigh Akha, A.A., C.M. Theriot, J.R. Erb-Downward, A.J. McDermott, N.R. Falkowski, H.M. Tyra, R.A. McDonald, D.T. Rutkowski, V.B. Young, G.B. Huffnagle. (2013) Acute Infection of Mice with Clostridium difficile Leads to an Innate Immune Response, eIF2α Phosphorylation and Pro-survival Signaling. Immunology. Sep; 140(1):111-122.

Theriot, C.M., C.K. Koumpouras, P.E. Carlson, I.L. Bergin, D.M. Aronoff, V.B. Young. (2011) Cefoperazone-treated Mice as an Experimental Platform to Assess Differential Virulence of Clostridium difficile Strains. Gut Microbes. 2(6): 326-334.



 
 
   
   

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