TY - JOUR
T1 - Enterococcus faecalis internalization in human umbilical vein endothelial cells (HUVEC).
AU - Millán, Diana
AU - Chiriboga, Carlos
AU - Patarroyo, Manuel A.
AU - Fontanilla, Marta R.
N1 - Funding Information:
We would like to thank Dr. Ricardo Sanchez for his assistance with the statistical analysis, Dr. Jinnethe Reyes and Dr. Martha Garzón for providing us with clinical isolates and Dr. Gary Dunny and Dr. Dawn A. Manias for providing OG1-SSpP11 and OG1-SSp strains, Dr. Diego Garzón and Dr. Andrea Castillo for their assistance with experimental assays and Jason Garry for reviewing English style and expression. This study was partly financed by Colciencias (contract 13080412635 ). We would like to dedicate this article to the loving memory of Doctor Carlos Chiriboga, a long-time friend who passed away recently.
Copyright:
Copyright 2017 Medline is the source for the citation and abstract of this record.
PY - 2013/4
Y1 - 2013/4
N2 - Initial Enterococcus faecalis-endothelial cell molecular interactions which lead to enterococci associating in the host endothelial tissue, colonizing it and proliferating there can be assessed using in vitro models. Cultured human umbilical vein endothelial cells (HUVEC) have been used to study other Gram-positive bacteria-cell interactions; however, few studies have been aimed at establishing the relationship of E. faecalis with endothelial cells. The aggregation substance (AS) family of adhesins represents an E. faecalis virulence factor which has been implicated in endocarditis severity and bacterial persistence. The Asc10 protein (a member of this family) promotes bacterium-bacterium aggregation and bacterium-host cell binding. Evaluating Asc10 role in bacterial internalization by cultured enterocytes has shown that this adhesin facilitates E. faecalis endocytosis by HT-29 cells. A few eukaryotic cell structural components, such as cytoskeletal proteins, have been involved in E. faecalis entry into cell-lines; it is thus relevant to determine whether Asc10, as well as microtubules and actin microfilaments, play a role in E. faecalis internalization by cultured endothelial cells. The role of Asc10 and cytoskeleton proteins in E. faecalis ability to enter HUVEC was assessed in the present study, as well as cell apoptosis induction by enterococcal internalization by HUVEC; the data indicated increased cell apoptosis and that cytoskeleton components were partially involved in E. faecalis entry to endothelial cells, thereby suggesting that E. faecalis Asc10 protein would not be a critical factor for bacterial entry to cultured HUVEC.
AB - Initial Enterococcus faecalis-endothelial cell molecular interactions which lead to enterococci associating in the host endothelial tissue, colonizing it and proliferating there can be assessed using in vitro models. Cultured human umbilical vein endothelial cells (HUVEC) have been used to study other Gram-positive bacteria-cell interactions; however, few studies have been aimed at establishing the relationship of E. faecalis with endothelial cells. The aggregation substance (AS) family of adhesins represents an E. faecalis virulence factor which has been implicated in endocarditis severity and bacterial persistence. The Asc10 protein (a member of this family) promotes bacterium-bacterium aggregation and bacterium-host cell binding. Evaluating Asc10 role in bacterial internalization by cultured enterocytes has shown that this adhesin facilitates E. faecalis endocytosis by HT-29 cells. A few eukaryotic cell structural components, such as cytoskeletal proteins, have been involved in E. faecalis entry into cell-lines; it is thus relevant to determine whether Asc10, as well as microtubules and actin microfilaments, play a role in E. faecalis internalization by cultured endothelial cells. The role of Asc10 and cytoskeleton proteins in E. faecalis ability to enter HUVEC was assessed in the present study, as well as cell apoptosis induction by enterococcal internalization by HUVEC; the data indicated increased cell apoptosis and that cytoskeleton components were partially involved in E. faecalis entry to endothelial cells, thereby suggesting that E. faecalis Asc10 protein would not be a critical factor for bacterial entry to cultured HUVEC.
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U2 - 10.1016/j.micpath.2012.11.007
DO - 10.1016/j.micpath.2012.11.007
M3 - Research Article
C2 - 23174630
AN - SCOPUS:85027931096
SN - 0882-4010
VL - 57
SP - 62
EP - 69
JO - Microbial Pathogenesis
JF - Microbial Pathogenesis
ER -