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Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins
Listeriosis is a severe disease caused by the opportunistic bacterial pathogen Listeria monocytogenes (L. monocytogenes). Previous studies indicate that of the four phylogenetical lineages known, lineage I strains are significantly more prevalent in clinical infections than in the environment. Among...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6612545/ https://www.ncbi.nlm.nih.gov/pubmed/30656829 http://dx.doi.org/10.1002/mbo3.790 |
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author | Gözel, Bulent Monney, Camille Aguilar‐Bultet, Lisandra Rupp, Sebastian Frey, Joachim Oevermann, Anna |
author_facet | Gözel, Bulent Monney, Camille Aguilar‐Bultet, Lisandra Rupp, Sebastian Frey, Joachim Oevermann, Anna |
author_sort | Gözel, Bulent |
collection | PubMed |
description | Listeriosis is a severe disease caused by the opportunistic bacterial pathogen Listeria monocytogenes (L. monocytogenes). Previous studies indicate that of the four phylogenetical lineages known, lineage I strains are significantly more prevalent in clinical infections than in the environment. Among lineage 1, sequence type (ST1) belongs to the most frequent genotypes in clinical infections and behaves hyperinvasive in experimental in vitro infections compared to lineage II strains suggesting that yet uncharacterized virulence genes contribute to high virulence of certain lineage I strains. This study investigated the effect of four specific lineage I genes encoding surface proteins with internalin‐like structures on cellular infection. CNS derived cell lines (fetal bovine brain cells, human microglia cells) and non‐CNS derived cell lines (bovine macrophage cells, human adenocarcinoma cells) that represent the various target cells of L. monocytogenes were infected with the parental ST1 strain and deletion mutants of the four genes. Despite their association with lineage I, deletion of the four genes investigated did not dampen the hyperinvasiveness of the ST1 strain. Similarly, these genes did not contribute to the intracellular survival and intercellular spread of L. monocytogenes ST1, indicating that these genes may have other functions, either during the infection process or outside the host. |
format | Online Article Text |
id | pubmed-6612545 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-66125452019-07-16 Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins Gözel, Bulent Monney, Camille Aguilar‐Bultet, Lisandra Rupp, Sebastian Frey, Joachim Oevermann, Anna Microbiologyopen Original Articles Listeriosis is a severe disease caused by the opportunistic bacterial pathogen Listeria monocytogenes (L. monocytogenes). Previous studies indicate that of the four phylogenetical lineages known, lineage I strains are significantly more prevalent in clinical infections than in the environment. Among lineage 1, sequence type (ST1) belongs to the most frequent genotypes in clinical infections and behaves hyperinvasive in experimental in vitro infections compared to lineage II strains suggesting that yet uncharacterized virulence genes contribute to high virulence of certain lineage I strains. This study investigated the effect of four specific lineage I genes encoding surface proteins with internalin‐like structures on cellular infection. CNS derived cell lines (fetal bovine brain cells, human microglia cells) and non‐CNS derived cell lines (bovine macrophage cells, human adenocarcinoma cells) that represent the various target cells of L. monocytogenes were infected with the parental ST1 strain and deletion mutants of the four genes. Despite their association with lineage I, deletion of the four genes investigated did not dampen the hyperinvasiveness of the ST1 strain. Similarly, these genes did not contribute to the intracellular survival and intercellular spread of L. monocytogenes ST1, indicating that these genes may have other functions, either during the infection process or outside the host. John Wiley and Sons Inc. 2019-01-17 /pmc/articles/PMC6612545/ /pubmed/30656829 http://dx.doi.org/10.1002/mbo3.790 Text en © 2019 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Gözel, Bulent Monney, Camille Aguilar‐Bultet, Lisandra Rupp, Sebastian Frey, Joachim Oevermann, Anna Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins |
title | Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins |
title_full | Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins |
title_fullStr | Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins |
title_full_unstemmed | Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins |
title_short | Hyperinvasiveness of Listeria monocytogenes sequence type 1 is independent of lineage I‐specific genes encoding internalin‐like proteins |
title_sort | hyperinvasiveness of listeria monocytogenes sequence type 1 is independent of lineage i‐specific genes encoding internalin‐like proteins |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6612545/ https://www.ncbi.nlm.nih.gov/pubmed/30656829 http://dx.doi.org/10.1002/mbo3.790 |
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