ArticleInfection and immunity1996
Analysis of epithelial cell stress response during infection by Shigella flexneri.
Article in Infection and immunity, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 75 citations in OpenAlex.
- Shigella flexneri Diguanylate Cyclases Regulate Virulence.Journal of bacteriology · 2021Article
- A Versatile Human Intestinal Organoid-Derived Epithelial Monolayer Model for the Study of Enteric Pathogens.Microbiology spectrum · 2021Article
- Cytosolic Gram-negative bacteria prevent apoptosis by inhibition of effector caspases through lipopolysaccharide.Nature microbiology · 2020Article
- Human Intestinal Enteroids as a Model System ofInfection and immunity · 2019Article
- Shigella Pathogenesis Modeling with Tissue Culture Assays.Current protocols in microbiology · 2018Article
- A Brief History ofEcoSal Plus · 2018Review
- Cellular Aspects of Shigella Pathogenesis: Focus on the Manipulation of Host Cell Processes.Frontiers in cellular and infection microbiology · 2016Review
- BID-dependent release of mitochondrial SMAC dampens XIAP-mediated immunity against Shigella.The EMBO journal · 2014Article
- Shigella reroutes host cell central metabolism to obtain high-flux nutrient supply for vigorous intracellular growth.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Functional identification of APIP as human mtnB, a key enzyme in the methionine salvage pathway.PloS one · 2012Article
- Interaction of enteric bacterial pathogens with murine embryonic stem cells.Infection and immunity · 2009Article
- Bacterial conjugation in the cytoplasm of mouse cells.Infection and immunity · 2008Article
- Shigella flexneri inhibits staurosporine-induced apoptosis in epithelial cells.Infection and immunity · 2007Article
- Apyrase, the product of the virulence plasmid-encoded phoN2 (apy) gene of Shigella flexneri, is necessary for proper unipolar IcsA localization and for efficient intercellular spread.Journal of bacteriology · 2006Article
- Transcriptional adaptation of Shigella flexneri during infection of macrophages and epithelial cells: insights into the strategies of a cytosolic bacterial pathogen.Infection and immunity · 2005Article
- Growth phase-regulated induction of Salmonella-induced macrophage apoptosis correlates with transient expression of SPI-1 genes.Journal of bacteriology · 1999Article
- Apoptosis of human intestinal epithelial cells after bacterial invasion.The Journal of clinical investigation · 1998Article
- Expression of the virulence plasmid-carried apyrase gene (apy) of enteroinvasive Escherichia coli and Shigella flexneri is under the control of H-NS and the VirF and VirB regulatory cascade.Infection and immunity · 1998Article
- Alteration of HLA-B27 peptide presentation after infection of transfected murine L cells by Shigella flexneri.Infection and immunity · 1998Article
- Clearance of Shigella flexneri infection occurs through a nitric oxide-independent mechanism.Infection and immunity · 1998Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shigella flexneri-infected macrophage cells undergo an apoptotic-like death as early as one hour after infection (A. Zychlinsky, M. C. Prévost, and P. J. Sansonetti, Nature [London] 358:167-168, 1992). To determine the fate of infected epithelial cells, we characterized the viability, morphology, and several metabolic activities of HeLa cells after treatment with M90T, an invoffve isolate of S. flexneri serotype 5, or BS176, a noninvasive isolate cured of the 220-kb virulence plasmid. Using standard assays, we found that for at least 4 h after infection with M90T, HeLa cells remained viable and did not detach or lyse. The ultrastructural morphology of HeLa cells heavily infected with M90T was free of hallmarks associated with cells undergoing apoptosis. Consistent with the idea that intracellular bacterial growth is metabolically stressful to the host cell, we observed that, compared with BS176 treated-HeLa cells, M90T-treated HeLa cells showed (i) a significant decrease in the total pool size of nucleoside triphosphates, (ii) a reduced ability to incorporate extracellular radiolabeled methionine into the soluble and insoluble cell fractions, and (iii) a stimulation of glucose uptake. However, there was no detectable increase in expression of the stress-inducible hsp70 gene in M90T-infected HeLa cells or activation of the anaerobic metabolic pathway as determined by measuring total lactate levels. These results demonstrate clearly that the fate of S.flexneri-infected cells can vary dramatically between cell types and agree with the hypothesis that the destruction of epithelial cells observed in experimental models of shigellosis is due to the host inflammatory response and probably not bacterial intracellular multiplication per se.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.