Investigation of Specific Substitutions in Virulence Genes Characterizing Phenotypic Groups of Low-Virulence Field Strains of
            <i>Listeria monocytogenes</i>

Roche, Sylvie; Gracieux, Patrice; Milohanic, Eliane; Albert, Isabelle; Virlogeux-Payant, Isabelle; Témoin, Stéphanie; Grépinet, Olivier; Kérouanton, Annaëlle; Jacquet, Christine; Cossart, Pascale; Velge, Philippe

doi:10.1128/aem.71.10.6039-6048.2005

Cited by 90 publications

(84 citation statements)

References 41 publications

(39 reference statements)

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“…We had previously identified 26 low-virulence field strains which were assigned to four groups (Roche et al, 2005). For five out of six strains in group III, the same mutations in three genes, plcA, inlA and inlB, were responsible for their inability to form plaques; this ability was restored by complementation with the corresponding genes of the virulent EGDe strain.…”

Section: Discussionmentioning

confidence: 99%

“…S2a) that led to three mutations in PI-PLC ( Supplementary Fig. S2b) (Roche et al, 2005). Analysis of the mutations showed that the isoleucine-valine substitution at position 17 (Ile17Val) was located in the signal sequence of the protein.…”

Section: Nucleotide Sequencing Of the Virulence Genesmentioning

confidence: 99%

“…Detection of PI-PLC activity was checked on PI-TY agar, as described elsewhere (Notermans et al, 1991), and was analysed in the culture supernatant with tritium-labelled L-aphosphatidyl-inositol, as previously described (Roche et al, 2005). Experiments were performed in triplicate for each strain.…”

Section: Strainmentioning

confidence: 99%

“…They also exhibited a low lethality in mice compared to virulent strains . These low-virulence strains, unrelated in origin and isolation date, were assigned to one of four groups based on their phenotypic characteristics, using cluster analysis (Roche et al, 2005). The cause of the low virulence of the 11 strains belonging to Group I has been identified.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2008

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In order to understand the causes of the low virulence of Listeria monocytogenes field strains, five low-virulence strains were analysed. These five strains showed changes in relation to invasion, phosphatidyl-inositol phospholipase C (PI-PLC) activity, plaque formation and in vivo virulence. Molecular analyses revealed the same mutations in the plcA, inlA and inlB genes in all five strains. The Thr262Ala substitution in the PI-PLC protein was responsible for the absence of PI-PLC activity. This residue, conserved in certain L. monocytogenes species, is located at the outer rim of the active site pocket and could impair the cleavage activity of the enzyme. The low invasion rate of these strains was due to a nonsense codon leading to a lack of InlA protein synthesis, and to an Ala117Thr substitution in the leucine-rich repeat of InlB, which altered the interaction with the Met receptor. Single trans complementation with the inlA EGDe , inlB EGDe or plcA EGDe genes restored the capacity of low-virulence strains either to enter epithelial and fibroblastic cells or to express PI-PLC activity. Complementation by allelic exchange of the plcA EGDe gene on the chromosome and trans complementation with either the inlA EGDe or the inlB EGDe gene restored the ability to form plaques, but only partly restored the in vivo virulence, suggesting that there were other gene mutation(s) with consequences that could mainly be observed in vivo. These results indicate that the low virulence of L. monocytogenes strains can be explained by point mutations in a number of virulence genes; these could therefore be important for detecting low-virulence strains. Moreover, the fact that all the strains had the same substitutions suggests that they have a common evolutionary pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Nucleotide Sequencing Of the Virulence Genesmentioning

confidence: 99%

Section: Strainmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2008

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“…Eight to 21% of strains are estimated to be avirulent or weakly virulent (Roche et al 2005). There is little information on pathogenicity of L. monocytogenes strains of animal origin.…”

Section: Discussionmentioning

confidence: 99%

Invasiveness of Listeria monocytogenes strains isolated from animals in Poland

Wałecka-Zacharska¹,

Kosek-Paszkowska²,

Bania³

et al. 2015

Polish Journal of Veterinary Sciences

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Animals are important reservoir of Listeria monocytogenes, a pathogen causing serious infections in both humans and livestock. However, data on invasiveness of L. monocytogenes strains of animal origin is very scarce. Ability of 18 L. monocytogenes strains of animal origin to invade HT-29 cells was investigated. Plaque forming assay was used to assess invasiveness and ability of the pathogen to spread in the cell line. Almost 40% of L. monocytogenes strains were weakly invasive. It was shown that strains from serogroup 4b exhibited the highest invasiveness, whereas serogroup 1/2b consisted of strains of invasiveness below 0.0001%. Analysis of translated inlA and inlB gene sequences revealed no premature stop codons. Lineage-specific mutations in low invasive strains were identified within inlA and inlB sequences. Our results demonstrate high incidence of low invasive animal L. monocytogenes strains, which may be at least partly explained by unique point mutations in the InlA and InlB.

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Animal Models of Listeria Infection

2008

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Listeria monocytogenes is an intracellular foodborne pathogen that causes listeriosis, an infection characterized by gastroenteritis, meningitis, encephalitis, and maternofetal infections in humans. L. monocytogenes enters the host via contaminated foods, invades the small intestine, translocates to mesenteric lymph nodes, and spreads to the liver, spleen, brain and, in pregnant women, the fetoplacental unit. Many pathogenicity tests for studying L. monocytogenes have been developed, including tests using laboratory animals. A number of small animal species can be experimentally infected with Listeria. Mice and guinea pigs can be infected either intragastrically or intravenously, and virulence evaluated either by enumerating bacteria within infected target organs or by evaluating the 50% lethal dose (LD50). Although mice and guinea pigs can be infected with Listeria by a variety of routes, the intragastric route is the most relevant to the human foodborne listeriosis.

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Investigation of Specific Substitutions in Virulence Genes Characterizing Phenotypic Groups of Low-Virulence Field Strains of Listeria monocytogenes

Cited by 90 publications

References 41 publications

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

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

Invasiveness of Listeria monocytogenes strains isolated from animals in Poland

Animal Models of Listeria Infection

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