Adhesion to the host cell surface is sufficient to mediateListeria monocytogenesentry into epithelial cells
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| Title: | Adhesion to the host cell surface is sufficient to mediateListeria monocytogenesentry into epithelial cells |
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| Authors: | Fabian E. Ortega, Natalie Chavez, Peter M. Lauer, William S. Luckett, W. James Nelson, Kathleen A. Siemers, Martijn Gloerich, Julie M. Bianchini, Julie A. Theriot, Michelle Rengarajan, Prathima Radhakrishnan |
| Contributors: | Cancer, CMM Groep Gloerich |
| Source: | Mol Biol Cell |
| Publisher Information: | American Society for Cell Biology (ASCB), 2017. |
| Publication Year: | 2017 |
| Subject Terms: | 0301 basic medicine, Cell Culture Techniques, Antigens, Surface/metabolism, Cadherins/immunology, Madin Darby Canine Kidney Cells, 03 medical and health sciences, Dogs, Bacterial Proteins, Cell Line, Tumor, Journal Article, Cell Adhesion, Actins/immunology, Animals, Humans, Cell Adhesion/physiology, Epithelial Cells/microbiology, Bacterial Proteins/metabolism, Cell Membrane/metabolism, Cell Membrane, Epithelial Cells, Articles, Cadherins, Listeria monocytogenes, Intercellular Junctions/metabolism, Actins, alpha Catenin/metabolism, Intercellular Junctions, 13. Climate action, Antigens, Surface, Listeria monocytogenes/metabolism, alpha Catenin |
| Description: | The intestinal epithelium is the first physiological barrier breached by the Gram-positive facultative pathogen Listeria monocytogenes during an in vivo infection. Listeria monocytogenes binds to the epithelial host cell receptor E-cadherin, which mediates a physical link between the bacterium and filamentous actin (F-actin). However, the importance of anchoring the bacterium to F-actin through E-cadherin for bacterial invasion has not been tested directly in epithelial cells. Here we demonstrate that depleting αE-catenin, which indirectly links E-cadherin to F-actin, did not decrease L. monocytogenes invasion of epithelial cells in tissue culture. Instead, invasion increased due to increased bacterial adhesion to epithelial monolayers with compromised cell–cell junctions. Furthermore, expression of a mutant E-cadherin lacking the intracellular domain was sufficient for efficient L. monocytogenes invasion of epithelial cells. Importantly, direct biotin-mediated binding of bacteria to surface lipids in the plasma membrane of host epithelial cells was sufficient for uptake. Our results indicate that the only requirement for L. monocytogenes invasion of epithelial cells is adhesion to the host cell surface, and that E-cadherin–mediated coupling of the bacterium to F-actin is not required. |
| Document Type: | Article Other literature type |
| File Description: | application/pdf |
| Language: | English |
| ISSN: | 1939-4586 1059-1524 |
| DOI: | 10.1091/mbc.e16-12-0851 |
| Access URL: | https://pubmed.ncbi.nlm.nih.gov/28877987 https://www.molbiolcell.org/content/28/22/2945.full https://www.molbiolcell.org/doi/full/10.1091/mbc.e16-12-0851 https://www.ncbi.nlm.nih.gov/pubmed/28877987 http://europepmc.org/articles/PMC5662255 https://dspace.library.uu.nl/handle/1874/457915 |
| Rights: | CC BY NC SA |
| Accession Number: | edsair.doi.dedup.....b9640b11b9f5f4edbce811dc53cf4d11 |
| Database: | OpenAIRE |
| Abstract: | The intestinal epithelium is the first physiological barrier breached by the Gram-positive facultative pathogen Listeria monocytogenes during an in vivo infection. Listeria monocytogenes binds to the epithelial host cell receptor E-cadherin, which mediates a physical link between the bacterium and filamentous actin (F-actin). However, the importance of anchoring the bacterium to F-actin through E-cadherin for bacterial invasion has not been tested directly in epithelial cells. Here we demonstrate that depleting αE-catenin, which indirectly links E-cadherin to F-actin, did not decrease L. monocytogenes invasion of epithelial cells in tissue culture. Instead, invasion increased due to increased bacterial adhesion to epithelial monolayers with compromised cell–cell junctions. Furthermore, expression of a mutant E-cadherin lacking the intracellular domain was sufficient for efficient L. monocytogenes invasion of epithelial cells. Importantly, direct biotin-mediated binding of bacteria to surface lipids in the plasma membrane of host epithelial cells was sufficient for uptake. Our results indicate that the only requirement for L. monocytogenes invasion of epithelial cells is adhesion to the host cell surface, and that E-cadherin–mediated coupling of the bacterium to F-actin is not required. |
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| ISSN: | 19394586 10591524 |
| DOI: | 10.1091/mbc.e16-12-0851 |
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