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Global impact of Salmonella type III secretion effector SteA on host cells

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>>
Publication Date:
Jul 11, 2014
Product Type:
Journal Article
Resource Relation:
Journal Name: Biochemical and Biophysical Research Communications; Journal Volume: 449; Journal Issue: 4; Other Information: Copyright (c) 2014 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; BIOLOGY; BIOTECHNOLOGY; CELL PROLIFERATION; FEVER; HELA CELLS; HUMAN POPULATIONS; LACTATE DEHYDROGENASE; METHACRYLATES; NUCLEOTIDES; PATHOGENS; PHOSPHORYLATION; POLYMERASE CHAIN REACTION; SALMONELLA; SECRETION; THREONINE; TOXICITY; TYPHOID; VIRULENCE
OSTI ID:
22416608
Country of Origin:
United States
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 0006-291X; CODEN: BBRCA9; Other: PII: S0006-291X(14)00928-0; TRN: US15R1229122500
Availability:
Available from http://dx.doi.org/10.1016/j.bbrc.2014.05.056
Submitting Site:
USN
Size:
page(s) 419-424
Announcement Date:
Jan 05, 2016

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. doi: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. doi:10.1016/J.BBRC.2014.05.056. https://www.osti.gov/servlets/purl/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 = {Biochemical and Biophysical Research Communications}
issue = {4}
volume = {449}
journal type = {AC}
place = {United States}
year = {2014}
month = {Jul}
}