ArticleBMC genomics2010
Microarray analysis of Shigella flexneri-infected epithelial cells identifies host factors important for apoptosis inhibition.
Article in BMC genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Pathogenicity and virulence ofVirulence · 2023Review
- Article
- A Versatile Human Intestinal Organoid-Derived Epithelial Monolayer Model for the Study of Enteric Pathogens.Microbiology spectrum · 2021Article
- To Study the Anti-cancer Effects of Shigella Flexneri in AspC-1 Pancreatic Cancer Cell Line in Approach to Bax and bcl-2 Genes.Journal of gastrointestinal cancer · 2021Article
- Human Intestinal Enteroids as a Model System ofInfection and immunity · 2019Article
- Eukaryotic pathways targeted by the type III secretion system effector protein, BipC, involved in the intracellular lifecycle of Burkholderia pseudomallei.Scientific reports · 2016Article
- Bacterial secreted effectors and caspase-3 interactions.Cellular microbiology · 2014Review
- DNA microarray-based gene expression profiling of estrogenic chemicals.Cellular and molecular life sciences : CMLS · 2014Review
- TolC-dependent modulation of host cell death by the Francisella tularensis live vaccine strain.Infection and immunity · 2014Article
- Systems-level overview of host protein phosphorylation during Shigella flexneri infection revealed by phosphoproteomics.Molecular & cellular proteomics : MCP · 2013Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundShigella flexneri inhibits apoptosis in infected epithelial cells. In order to understand the pro-survival effects induced by the bacteria, we utilized apoptosis-specific microarrays to analyze the changes in eukaryotic gene expression in both infected and uninfected cells in the presence and absence of staurosporine, a chemical inducer of the intrinsic pathway of apoptosis. The goal of this research was to identify host factors that contribute to apoptosis inhibition in infected cells.
resultsThe microarray analysis revealed distinct expression profiles in uninfected and infected cells, and these changes were altered in the presence of staurosporine. These profiles allowed us to make comparisons between the treatment groups. Compared to uninfected cells, Shigella-infected epithelial cells, both in the presence and absence of staurosporine, showed significant induced expression of JUN, several members of the inhibitor of apoptosis gene family, nuclear factor kappaB and related genes, genes involving tumor protein 53 and the retinoblastoma protein, and surprisingly, genes important for the inhibition of the extrinsic pathway of apoptosis. We confirmed the microarray results for a selection of genes using in situ hybridization analysis.
conclusionInfection of epithelial cells with S. flexneri induces a pro-survival state in the cell that results in apoptosis inhibition in the presence and absence of staurosporine. The bacteria may target these host factors directly while some induced genes may represent downstream effects due to the presence of the bacteria. Our results indicate that the bacteria block apoptosis at multiple checkpoints along both pathways so that even if a cell fails to prevent apoptosis at an early step, Shigella will block apoptosis at the level of caspase-3. Apoptosis inhibition is most likely vital to the survival of the bacteria in vivo. Future characterization of these host factors is required to fully understand how S. flexneri inhibits apoptosis in epithelial cells.
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