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United States Department of Agriculture

Agricultural Research Service

Research Project: VALIDATION OF THE EFFECT OF INTERVENTIONS AND PROCESSES ON PERSISTENCE OF PATHOGENS ON FOODS Title: The role of gtcA in the pathogenesis of gastrointestinal listeriosis

Authors
item Faith, Nancy - UNIV. OF WISCONSIN
item Kathariou, Sophia - N.C. STATE UNIV.
item Shi, Lewis - UNIV. OF WISCONSIN
item Drevets, Doug - UNIV. OF OKLAHOMA
item Shaghian, Robert - UNIV. OF WISCONSIN
item Neudeck, Brien - UNIV. TENN. MED CTR.
item Luchansky, John
item Czuprynski, Charles - UNIV. OF WISCONSIN

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: September 26, 2008
Publication Date: September 28, 2008
Citation: Faith,N.,Kathariou,S.,Shi,L.,Drevets,D.,Shaghian,R.,Neudeck,B.,Luchansky,J.,Czuprynski,C. 2008. The role of gtca in the pathogenesis of gastrointestinal listeriosis [abstract]. Midwest Pathogenesis Meeting. Madison,WS. p.1.

Technical Abstract: Serotype 4b strains of Listeria monocytogenes have been implicated in most large outbreaks of listeriosis. The reason for this relationship remains unclear. The gtcA gene is required for glycosylation of teichoic acid on serotype 4b L. monocytogenes. In this study, we investigated two different serotype 4b mutants of gtcA, which lack glucose and galactose residues on their teichoic acid, for their virulence when inoculated intragastrically into anesthetized A/J mice. Both gtcA mutant strains were recovered in lesser numbers from the spleen, liver, ceca and gall bladders of mice inoculated i.g. than were their respective parent strains of L. monocytogenes. We observed a difference in resistance to synthetic gastric fluid (pH 4.5) between gtcA mutants and the associated parent strains. gtcA mutants of L. monocytogenes were less able to invade the Caco-2 human intestinal epithelial cell line, and were lesser in number after a 24 hr incubation in vitro, than the respective wild type parent strains. However, we noted no significant difference in attachment of gtcA mutant and wild type L. monocytogenes to Caco-2 cells. In contrast, gtcA mutants of L. monocytogenes invaded the TIB73 murine embryonic hepatocyte cell line to a comparable level as wild type L. monocytogenes, but exhibited a diminished ability to multiply within TIB73 cells. We observed decreased expression of adhesion molecules (E-selectin, ICAM-1, VCAM-1) by human umbilical vein endothelial cells incubated with gtcA mutant than wild type L. monocytogenes. This response was not reflected in a decreased ability to invade HUVEC cells in vitro. We observed no significant difference between the ability of gtcA mutant and wild type L. monocytogenes to invade and multiply within RAW264.7 and J774 murine macrophage cell lines. We also investigated the impact of gtcA on selected attributes of relevance to food contamination by L. monocytogenes. In soft agar motility assays, both mutants exhibited reduced swarming. However, inactivation of gtcA was accompanied with decreased adherence to plastic (i.e. biofilm) only in the epidemic-associated strain. These findings indicate that in serotype 4b L. monocytogenes, gtcA is important in several characteristics relevant to pathogenesis and to contamination of foods, although the impact of the gene on some attributes is strain-specific.

Last Modified: 10/24/2014
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