Abstract
Highlights: • We analyzed HeLa cells transcriptome in response to Salmonella SteA. • Significant differential expression was detected for 58 human genes. • They are involved in ECM organization and regulation of some signaling pathways. • Cell death, cell adhesion and cell migration were decreased in SteA-expressing cells. • These results contribute to understand the role of SteA during infections. - Abstract: Salmonella enterica is a Gram-negative bacterium that causes gastroenteritis, bacteremia and typhoid fever in several animal species including humans. Its virulence is greatly dependent on two type III secretion systems, encoded in pathogenicity islands 1 and 2. These systems translocate proteins called effectors into eukaryotic host cell. Effectors interfere with host signal transduction pathways to allow the internalization of pathogens and their survival and proliferation inside vacuoles. SteA is one of the few Salmonella effectors that are substrates of both type III secretion systems. Here, we used gene arrays and bioinformatics analysis to study the genetic response of human epithelial cells to SteA. We found that constitutive synthesis of SteA in HeLa cells leads to induction of genes related to extracellular matrix organization and regulation of cell proliferation and serine/threonine kinase signaling pathways. SteA also causes repression of
More>>
Citation Formats
Cardenal-Muñoz, Elena, Gutiérrez, Gabriel, and Ramos-Morales, Francisco.
Global impact of Salmonella type III secretion effector SteA on host cells.
United States: N. p.,
2014.
Web.
doi:10.1016/J.BBRC.2014.05.056.
Cardenal-Muñoz, Elena, Gutiérrez, Gabriel, & Ramos-Morales, Francisco.
Global impact of Salmonella type III secretion effector SteA on host cells.
United States.
https://doi.org/10.1016/J.BBRC.2014.05.056
Cardenal-Muñoz, Elena, Gutiérrez, Gabriel, and Ramos-Morales, Francisco.
2014.
"Global impact of Salmonella type III secretion effector SteA on host cells."
United States.
https://doi.org/10.1016/J.BBRC.2014.05.056.
@misc{etde_22416608,
title = {Global impact of Salmonella type III secretion effector SteA on host cells}
author = {Cardenal-Muñoz, Elena, Gutiérrez, Gabriel, and Ramos-Morales, Francisco}
abstractNote = {Highlights: • We analyzed HeLa cells transcriptome in response to Salmonella SteA. • Significant differential expression was detected for 58 human genes. • They are involved in ECM organization and regulation of some signaling pathways. • Cell death, cell adhesion and cell migration were decreased in SteA-expressing cells. • These results contribute to understand the role of SteA during infections. - Abstract: Salmonella enterica is a Gram-negative bacterium that causes gastroenteritis, bacteremia and typhoid fever in several animal species including humans. Its virulence is greatly dependent on two type III secretion systems, encoded in pathogenicity islands 1 and 2. These systems translocate proteins called effectors into eukaryotic host cell. Effectors interfere with host signal transduction pathways to allow the internalization of pathogens and their survival and proliferation inside vacuoles. SteA is one of the few Salmonella effectors that are substrates of both type III secretion systems. Here, we used gene arrays and bioinformatics analysis to study the genetic response of human epithelial cells to SteA. We found that constitutive synthesis of SteA in HeLa cells leads to induction of genes related to extracellular matrix organization and regulation of cell proliferation and serine/threonine kinase signaling pathways. SteA also causes repression of genes related to immune processes and regulation of purine nucleotide synthesis and pathway-restricted SMAD protein phosphorylation. In addition, a cell biology approach revealed that epithelial cells expressing steA show altered cell morphology, and decreased cytotoxicity, cell–cell adhesion and migration.}
doi = {10.1016/J.BBRC.2014.05.056}
journal = []
issue = {4}
volume = {449}
journal type = {AC}
place = {United States}
year = {2014}
month = {Jul}
}
title = {Global impact of Salmonella type III secretion effector SteA on host cells}
author = {Cardenal-Muñoz, Elena, Gutiérrez, Gabriel, and Ramos-Morales, Francisco}
abstractNote = {Highlights: • We analyzed HeLa cells transcriptome in response to Salmonella SteA. • Significant differential expression was detected for 58 human genes. • They are involved in ECM organization and regulation of some signaling pathways. • Cell death, cell adhesion and cell migration were decreased in SteA-expressing cells. • These results contribute to understand the role of SteA during infections. - Abstract: Salmonella enterica is a Gram-negative bacterium that causes gastroenteritis, bacteremia and typhoid fever in several animal species including humans. Its virulence is greatly dependent on two type III secretion systems, encoded in pathogenicity islands 1 and 2. These systems translocate proteins called effectors into eukaryotic host cell. Effectors interfere with host signal transduction pathways to allow the internalization of pathogens and their survival and proliferation inside vacuoles. SteA is one of the few Salmonella effectors that are substrates of both type III secretion systems. Here, we used gene arrays and bioinformatics analysis to study the genetic response of human epithelial cells to SteA. We found that constitutive synthesis of SteA in HeLa cells leads to induction of genes related to extracellular matrix organization and regulation of cell proliferation and serine/threonine kinase signaling pathways. SteA also causes repression of genes related to immune processes and regulation of purine nucleotide synthesis and pathway-restricted SMAD protein phosphorylation. In addition, a cell biology approach revealed that epithelial cells expressing steA show altered cell morphology, and decreased cytotoxicity, cell–cell adhesion and migration.}
doi = {10.1016/J.BBRC.2014.05.056}
journal = []
issue = {4}
volume = {449}
journal type = {AC}
place = {United States}
year = {2014}
month = {Jul}
}