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Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae

Caveolae are 25–100 nm flask-like membrane structures enriched in cholesterol and glycosphingolipids. Researchers have proposed that Campylobacter jejuni require caveolae for cell invasion based on the finding that treatment of cells with the cholesterol-depleting compounds filipin III or methyl-β-c...

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Autores principales: Konkel, Michael E, Samuelson, Derrick R, Eucker, Tyson P, Shelden, Eric A, O'Loughlin, Jason L
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880046/
https://www.ncbi.nlm.nih.gov/pubmed/24364863
http://dx.doi.org/10.1186/1478-811X-11-100
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author Konkel, Michael E
Samuelson, Derrick R
Eucker, Tyson P
Shelden, Eric A
O'Loughlin, Jason L
author_facet Konkel, Michael E
Samuelson, Derrick R
Eucker, Tyson P
Shelden, Eric A
O'Loughlin, Jason L
author_sort Konkel, Michael E
collection PubMed
description Caveolae are 25–100 nm flask-like membrane structures enriched in cholesterol and glycosphingolipids. Researchers have proposed that Campylobacter jejuni require caveolae for cell invasion based on the finding that treatment of cells with the cholesterol-depleting compounds filipin III or methyl-β-cyclodextrin (MβCD) block bacterial internalization in a dose-dependent manner. The purpose of this study was to determine the role of caveolae and caveolin-1, a principal component of caveolae, in C. jejuni internalization. Consistent with previous work, we found that the treatment of HeLa cells with MβCD inhibited C. jejuni internalization. However, we also found that the treatment of HeLa cells with caveolin-1 siRNA, which resulted in greater than a 90% knockdown in caveolin-1 protein levels, had no effect on C. jejuni internalization. Based on this observation we performed a series of experiments that demonstrate that MβCD acts broadly, disrupting host cell lipid rafts and C. jejuni-induced cell signaling. More specifically, we found that MβCD inhibits the cellular events necessary for C. jejuni internalization, including membrane ruffling and Rac1 GTPase activation. We also demonstrate that MβCD disrupted the association of the β(1) integrin and EGF receptor, which are required for the maximal invasion of epithelial cells. In agreement with these findings, C. jejuni were able to invade human Caco-2 cells, which are devoid of caveolae, at a level equal to that of HeLa cells. Taken together, the results of our study demonstrate that C. jejuni internalization occurs in a caveolae-independent manner.
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spelling pubmed-38800462014-01-04 Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae Konkel, Michael E Samuelson, Derrick R Eucker, Tyson P Shelden, Eric A O'Loughlin, Jason L Cell Commun Signal Research Caveolae are 25–100 nm flask-like membrane structures enriched in cholesterol and glycosphingolipids. Researchers have proposed that Campylobacter jejuni require caveolae for cell invasion based on the finding that treatment of cells with the cholesterol-depleting compounds filipin III or methyl-β-cyclodextrin (MβCD) block bacterial internalization in a dose-dependent manner. The purpose of this study was to determine the role of caveolae and caveolin-1, a principal component of caveolae, in C. jejuni internalization. Consistent with previous work, we found that the treatment of HeLa cells with MβCD inhibited C. jejuni internalization. However, we also found that the treatment of HeLa cells with caveolin-1 siRNA, which resulted in greater than a 90% knockdown in caveolin-1 protein levels, had no effect on C. jejuni internalization. Based on this observation we performed a series of experiments that demonstrate that MβCD acts broadly, disrupting host cell lipid rafts and C. jejuni-induced cell signaling. More specifically, we found that MβCD inhibits the cellular events necessary for C. jejuni internalization, including membrane ruffling and Rac1 GTPase activation. We also demonstrate that MβCD disrupted the association of the β(1) integrin and EGF receptor, which are required for the maximal invasion of epithelial cells. In agreement with these findings, C. jejuni were able to invade human Caco-2 cells, which are devoid of caveolae, at a level equal to that of HeLa cells. Taken together, the results of our study demonstrate that C. jejuni internalization occurs in a caveolae-independent manner. BioMed Central 2013-12-23 /pmc/articles/PMC3880046/ /pubmed/24364863 http://dx.doi.org/10.1186/1478-811X-11-100 Text en Copyright © 2013 Konkel et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research
Konkel, Michael E
Samuelson, Derrick R
Eucker, Tyson P
Shelden, Eric A
O'Loughlin, Jason L
Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae
title Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae
title_full Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae
title_fullStr Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae
title_full_unstemmed Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae
title_short Invasion of epithelial cells by Campylobacter jejuni is independent of caveolae
title_sort invasion of epithelial cells by campylobacter jejuni is independent of caveolae
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880046/
https://www.ncbi.nlm.nih.gov/pubmed/24364863
http://dx.doi.org/10.1186/1478-811X-11-100
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