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ARS Home » Northeast Area » Beltsville, Maryland (BARC) » Beltsville Agricultural Research Center » Environmental Microbial & Food Safety Laboratory » Research » Publications at this Location » Publication #320701

Title: Understanding the host-adapted state of Citrobacter rodentium by transcriptomic analysis

item Smith, Allen
item Yan, Xianghe
item Chen, Celine
item Dawson, Harry
item Bhagwat, Arvind

Submitted to: Archives of Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/12/2016
Publication Date: 2/2/2016
Citation: Smith, A.D., Yan, X., Chen, C.T., Dawson, H.D., Bhagwat, A.A. 2016. Understanding the host-adapted state of Citrobacter rodentium by transcriptomic analysis. Archives Of Microbiology. 198:353-362.

Interpretive Summary: Transmission of pathogens in food-borne diarrheal outbreaks can occur via the fecal-oral route. Recent studies have documented that strains isolated directly from feces can exhibit enhanced virulence and infectivity. This increase in the disease causing potential of food-borne pathogens presents a formidable challenge for epidemiological investigations. Citrobacter rodentium is a mouse pathogen that mimics many aspects of enterohemorrhagic E. coli O157:H7 infection of humans, and serves as a useful model for studying virulence mechanisms. It develops a hyperinfectious state as it passes through the mouse gastrointestinal tract. We analyzed the entire transcriptome (total RNA) of C. rodentium while it was expressing enhanced virulence. Genes that enable cells to express critical adhesion proteins were highly expressed. In addition, several genes which regulate virulence were also identified. Developing tools to identify traits of hyper-virulent outbreak strains should provide a better measure of causality and associated food safety risks. This information will be of interest to other scientists and regulatory agencies.

Technical Abstract: Citrobacter rodentium (Cr) is a mouse pathogen that mimics many aspects of enteropathogenic Escherichia coli infections including producing attaching and effacing (A/E) lesions. Host-adapted (HA) Cr cells that are shed at the peak of infection have been reported to be hyperinfective. The exact mechanism underlying this phenomenon has remained elusive since the pathogen loses it’s HA ‘status’ immediately upon sub-culturing in laboratory media. Sequencing the entire transcriptome from the feces of infected mouse and media grown Cr, we and looked for differentially expressed Cr genes. We observed that the entire transcriptional machinery as well as several transcriptional regulators to be differentially expressed. Major adhesion and effector genes, tir and eae were highly expressed in HA along with many genes located on all five loci of enterocyte effacement regions (LEE 1-5). Notable absent among the HA expressed genes were 19 fimbrial operons and non-fimbrial adhesions and several non-LEE encoded effectors.