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Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪
The bacterial pathogen, Listeria monocytogenes, grows in the cytoplasm of host cells and spreads intercellularly using a form of actin-based motility mediated by the bacterial protein ActA. Tightly adherent monolayers of MDCK cells that constitutively express GFP-actin were infected with L. monocyto...
Autores principales: | , , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1999
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785326/ https://www.ncbi.nlm.nih.gov/pubmed/10491395 |
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author | Robbins, Jennifer R. Barth, Angela I. Marquis, Hélène de Hostos, Eugenio L. Nelson, W. James Theriot, Julie A. |
author_facet | Robbins, Jennifer R. Barth, Angela I. Marquis, Hélène de Hostos, Eugenio L. Nelson, W. James Theriot, Julie A. |
author_sort | Robbins, Jennifer R. |
collection | PubMed |
description | The bacterial pathogen, Listeria monocytogenes, grows in the cytoplasm of host cells and spreads intercellularly using a form of actin-based motility mediated by the bacterial protein ActA. Tightly adherent monolayers of MDCK cells that constitutively express GFP-actin were infected with L. monocytogenes, and intercellular spread of bacteria was observed by video microscopy. The probability of formation of membrane-bound protrusions containing bacteria decreased with host cell monolayer age and the establishment of extensive cell-cell contacts. After their extension into a recipient cell, intercellular membrane-bound protrusions underwent a period of bacterium-dependent fitful movement, followed by their collapse into a vacuole and rapid vacuolar lysis. Actin filaments in protrusions exhibited decreased turnover rates compared with bacterially associated cytoplasmic actin comet tails. Recovery of motility in the recipient cell required 1–2 bacterial generations. This delay may be explained by acid-dependent cleavage of ActA by the bacterial metalloprotease, Mpl. Importantly, we have observed that low levels of endocytosis of neighboring MDCK cell surface fragments occurs in the absence of bacteria, implying that intercellular spread of bacteria may exploit an endogenous process of paracytophagy. |
format | Text |
id | pubmed-1785326 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1999 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-17853262008-05-01 Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪ Robbins, Jennifer R. Barth, Angela I. Marquis, Hélène de Hostos, Eugenio L. Nelson, W. James Theriot, Julie A. J Cell Biol Original Article The bacterial pathogen, Listeria monocytogenes, grows in the cytoplasm of host cells and spreads intercellularly using a form of actin-based motility mediated by the bacterial protein ActA. Tightly adherent monolayers of MDCK cells that constitutively express GFP-actin were infected with L. monocytogenes, and intercellular spread of bacteria was observed by video microscopy. The probability of formation of membrane-bound protrusions containing bacteria decreased with host cell monolayer age and the establishment of extensive cell-cell contacts. After their extension into a recipient cell, intercellular membrane-bound protrusions underwent a period of bacterium-dependent fitful movement, followed by their collapse into a vacuole and rapid vacuolar lysis. Actin filaments in protrusions exhibited decreased turnover rates compared with bacterially associated cytoplasmic actin comet tails. Recovery of motility in the recipient cell required 1–2 bacterial generations. This delay may be explained by acid-dependent cleavage of ActA by the bacterial metalloprotease, Mpl. Importantly, we have observed that low levels of endocytosis of neighboring MDCK cell surface fragments occurs in the absence of bacteria, implying that intercellular spread of bacteria may exploit an endogenous process of paracytophagy. The Rockefeller University Press 1999-09-20 /pmc/articles/PMC1785326/ /pubmed/10491395 Text en © 1999 The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Original Article Robbins, Jennifer R. Barth, Angela I. Marquis, Hélène de Hostos, Eugenio L. Nelson, W. James Theriot, Julie A. Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪ |
title |
Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪ |
title_full |
Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪ |
title_fullStr |
Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪ |
title_full_unstemmed |
Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪ |
title_short |
Listeria monocytogenes Exploits Normal Host Cell Processes to Spread from Cell to Cell✪ |
title_sort | listeria monocytogenes exploits normal host cell processes to spread from cell to cell✪ |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1785326/ https://www.ncbi.nlm.nih.gov/pubmed/10491395 |
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