A Molecular Marker for Evaluating the Pathogenic Potential of FoodborneListeria monocytogenes

Abstract

This study demonstrates the critical role of internalin in the pathogenesis of human listeriosis. It provides a molecular explanation for the predominance of serovar 4b among clinical strains and supports the usefulness of studying the expression of internalin as a marker of virulence in humans.

Multiple point mutations in virulence genes explain the low virulence of Listeria monocytogenes field strains

“…Our PFA test on HT-29 cells combined with inoculation of mice allowed 8-20 % of low-virulence strains to be detected. However, strains exhibiting only an inactive InlA were not detected by our test, although 35 % of L. monocytogenes strains could have a truncated form of InlA and could thus be considered to be low-virulence strains (Olier et al, 2003;Jacquet et al, 2004). Moreover, numerous reports have demonstrated that non-haemolytic strains are avirulent, although the number of these strains is unknown, since many of them are not identified as L. monocytogenes strains when detection is based only on their haemolytic activity (Gaillard et al, 1986; Kathariou et al, 1987; Cossart et al, 1989).…”

Concepts and Mechanisms: Crossing Host Barriers

“…In contrast to nontransgenic mice, and similarly to guinea pigs and humans, transgenic mice expressing human E-cadherin are highly permissive to orally acquired listeriosis, demonstrating a critical role for InlA in the ability of L. monocytogenes to cross the intestinal barrier. Epidemiological study of human cases of listeriosis evidence supports this result, because clinical strains express a functional InlA significantly more often (96%) than food isolates do (65%) (Jacquet et al 2004), which is in favor of a role of InlA in crossing the intestinal barrier in humans. In contrast to the InlA-E-cadherin interaction, the InlB -Met interaction is not necessary for crossing the intestinal barrier in transgenic mice, as well as in gerbil, which is permissive for InlA and InlB (Khelef et al 2006;Disson et al 2008).…”

“…Of note, infection of fetus and abortion because of L. monocytogenes occur far more frequently during later stages of pregnancy ( 80% of maternofetal listeriosis occur after 22 weeks of amenorrhea; data from the French National Reference Center for Listeria). The requirement of InlA in L. monocytogenes crossing of the placental barriers has been independently shown epidemiologically, because L. monocytogenes isolates expressing a functional InlA are very significantly associated with their fetoplacental origin (Jacquet et al 2004;Disson et al 2008). The mechanism of infection has also been studied in animal models in vivo.…”

The arsenal of virulence factors deployed byListeria monocytogenesto promote its cell infection cycle

“…69 Epidemiological studies showed that InlA plays a key role in human listeriosis: 96% of clinical strains express a full-length functional form of InlA, while only 65% of food-isolated strains contained the fulllength form. 70 InlA/E-cadherin interaction is critical for epithelial cell invasion, as it activates complex signaling pathways leading to cytoskeletal reorganization. The E-cadherin extracellular domain is sufficient to promote InlA-dependent adherence, while the intracellular domain binding to catenins is required for the internalization process.…”