Rupp, Sebastian Dominic Alexander; Bärtschi, Michelle; Frey, Joachim; Oevermann, Anna (2017). Hyperinvasiveness and increased intercellular spread of Listeria monocytogenes sequence type 1 are independent of listeriolysin S, internalin F and internalin J1. Journal of medical microbiology, 66(7), pp. 1053-1062. SGM 10.1099/jmm.0.000529
Full text not available from this repository. (Request a copy)PURPOSE
Listeria monocytogenes is a genetically heterogeneous species, which is divided into evolutionary lineages and clonal complexes (CCs). Not all L. monocytogenes isolates are equally likely to cause disease, with CC1, and in particular sequence type (ST) 1, being the most prevalent complex in human and ruminant infections and more specifically in neurolisteriosis. While the major factors that determine neurotropism are unknown, the L. monocytogenes CC1 strains harbour listeriolysin S (lls) and particular alleles of internalin (inl) F and inlJ, which are not present in CCs commonly isolated from food and the environment. The aim of this study was to analyse the role of these factors in cellular infection.
METHODOLOGY
A ST1 field strain (JF5203) from CC1 isolated from a bovine rhombencephalitis case was used to create deletion mutants. These were tested alongside the parental strain and EGD-e (CC9), in different culture models representing L. monocytogenes targets (neurons, microglia, placenta, intestine and macrophages). The phenotype was assessed by quantification of c.f.u. from cell lysates and immunofluorescence analysis.
RESULTS
Compared to EGD-e, the ST1 strain JF5203 was hyperinvasive and exhibited increased intercellular spread. However, deletion of llsB, inlF or inlJ1, had no significant effect on infection or growth in the culture models tested.
CONCLUSION
Our results underline the importance of using relevant clinical strains when investigating L. monocytogenes virulence. We show that despite the association with CC1, llsB, inlF and inlJ1 are not involved in the hyperinvasiveness and efficient intercellular spread of ST1 in various cell types.
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