Comparison of the major virulence-related genes of Listeria monocytogenes in Internalin A truncated strain 36-25-1 and a clinical wild-type strain

Abstract

BackgroundInternalin A (InlA) facilitates the invasion of Listeria monocytogenes into a host cell. Some strains of Listeria monocytogenes express truncated forms of InlA, which reduces invasiveness. However, few virulence-related genes other than inlA have been analyzed in InlA-truncated strains. In the present study, we sequenced the draft genome of strain 36-25-1, an InlA-truncated strain, with pyrosequencing and compared 36 major virulence-related genes in this strain and a clinical wild-type strain.ResultsStrain 36-25-1 possessed all of the virulence-related genes analyzed. Of the analyzed genes, only 4 genes (dltA, gtcA, iap, and inlA) differed when the nucleotide sequences of strain 36-25-1 and the clinical wild-type strain were compared. Analysis of the deduced amino acid sequences found no mutations that significantly influenced virulence in genes other than inlA.ConclusionsThe virulence-associated genes in strain 36-25-1 differ little from those of the clinical wild-type strain, indicating that a slight mutation in the nucleotide sequence determines the virulence of the InlA-truncated strain. In addition, the results suggest that, aside from InlA-mediated cell invasiveness, there is almost no difference between the virulence of strain 36-25-1 and that of the clinical wild-type strain.

Secretome profiling of Propionibacterium freudenreichii reveals highly variable responses even among the closely related strains

“…Strain-specific differences in secretion of putative adhesins, including InlA, as well as that the role of phase-variation-like sequences leading to truncated adhesins, have also been reported to occur in C. acnes (Holland et al, 2010). Truncation of InlA due to a nonsense mutation is also common in some other bacterial pathogens, in which the InlA variant has been associated with reduced invasiveness (Kyoui et al, 2014). Thus, our findings imply that InlA could have been the target of adaptive modification in propionibacteria.…”

A review of Listeria monocytogenes from meat and meat products: Epidemiology, virulence factors, antimicrobial resistance and diagnosis

“…Escaping from both layers of vacuole membranes is important for an effective infection, and failure to escape the membrane results in an infection that is removed fast from the tissues (Pushkareva & Ermolaeva 2010 ). The haemolysin ( hly ), gene, is responsible for producing a pore-forming surface toxin called LLO, which is required for lysis of vacuole membranes and the release of L. monocytogenes into cytoplasm (Kyoui et al 2014 ). The absence of LLO equals avirulent strains of L. monocytogenes as the bacterium will not reach the cytoplasm (Pushkareva & Ermolaeva 2010 ); thus, it can be said that LLO is secreted by all virulent strains of L. monocytogenes .…”

Prevalence, virulence characterization, and genetic relatedness of Listeria monocytogenes isolated from chicken retail points and poultry slaughterhouses in Turkey

“…Virulence genes such as dltA, plcA, plcB, mpl, and actA were detected using the same PCR conditions described in Table 1 [36,[39][40][41][42][43]. The internalin genes (inlA, inlC, and inlJ) and other virulence factor genes (hylA, prfA, fri, and flaA) were determined using the modified PCR conditions shown in Table 1.…”