Submitted to: Foodborne Pathogens and Disease
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/1/2008
Publication Date: 2/1/2009
Citation: Faith, N., Kathariou, S., Promadej, N., Neudeck, B.L., Zhang, Q., Luchansky, J.B., Czuprynski, C. 2009. The role of gtcA in the pathogenesis of gastrointestinal listeriosis in mice. Foodborne Pathogens and Disease. 6:39-48. Interpretive Summary: Among food borne pathogens, Listeria monocytogenes is of particular concern due to its ubiquity in the food supply, as well as the severity of listeriosis and the economic burden of product recalls due to contamination with listeriae. As for other bacteria, listeriae display certain sugars on their outer surface, some of which may contribute to the pathogenicity and/or persistence of this bacterium in foods or people. In this study we investigated whether genes contributing to the presence/absence of target sugar groups on the surface of L. monocytogenes play a role in gastrointestinal listeriosis. In comparison to the parental strain, a mutant deficient in a gene designated gtcA was recovered in lower numbers from the spleen, liver, and other internal organs/tissues of mice. Likewise, the gtcA mutant was less invasive in a human cell line. These data suggest that the gtcA gene is an important contributor to the virulence of L. monocytogenes.
Technical Abstract: Serotype 4b strains of Listeria monocytogenes have been responsible for most large outbreaks of listeriosis. In L. monocytogenes serotype 4b, gtcA and gltA have been implicated in serotype-specific glycosylation of the teichoic acid of the cell wall with galactose and glucose. In this study, we investigated the impact of mutations in gltA (resulting in absence of glucose on teichoic acid) and gtcA (resulting in absence of galactose, and markedly reduced glucose on teichoic acid) on virulence following intragastric infection of anesthetized A=J mice. The gltA mutant was not impaired in virulence in this model. In contrast, testing of gtcA mutants constructed in two different strains showed that the mutants were recovered in lower numbers than their respective parent strains from the spleen, liver, ceca, and gall bladders of intragastrically inoculated mice. Genetic complementation of the gtcA mutation partially restored gastrointestinal virulence. When mice were inoculated intravenously, the gtcA mutants were also recovered in lower numbers from the liver (for both mutant strains) and the spleen (for one mutant strain) than their respective parental strains. The mutants were also evaluated for invasion and intracellular multiplication in the Caco-2 human intestinal epithelial cell line. Inactivation of gltA did not affect invasion or intracellular growth of the bacteria. In contrast, gtcA mutants showed decreased invasion, but normal multiplication in Caco-2 cells. Overall, these data demonstrate a role for gtcA in the pathogenesis of gastrointestinal listeriosis in mice, and suggest that diminished ability of gtcA mutants to invade intestinal epithelial cells may be partly responsible for decreased gastrointestinal virulence.