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

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 (T3SSs), encoded in pathogenicity islands 1 (SPI1) and 2 (SPI2), respectively. These systems translocate proteins called effectors into eukaryotic host cell. Effectors interfere with certain 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 T3SSs. Nothing is known about the function of this protein inside the host cells. 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 epithelial cells leads to induction of genes related to extracellular matrix organization and regulation of cell proliferation and serine/threonine kinase signaling pathways. SteA also represses genes related to immune processes and regulation of purine nucleotide synthesis and pathway-restricted SMAD protein phosphorylation. Consisted with this analysis a cell biology approach revealed that epithelial cells expressing steA show altered cell morphology, reduction of cytotoxicity, cell-cell adhesion and migration capability, and increase in endocytosis. Three experiments. Each experiment replicated three times. Control: HeLa cell transfected with plasmid pBABE without steA, Experiment 1:HeLa line 2 transfected with plasmid pBABE with steA. Experiment 2: HeLa line 4 transfected with plasmid pBABE with steA

ORGANISM(S): Homo sapiens

SUBMITTER: Gabriel Gutierrez 

PROVIDER: E-GEOD-51043 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress