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.