ArticleInfection and immunity2012
Hierarchies of host factor dynamics at the entry site of Shigella flexneri during host cell invasion.
Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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
17 citing papers in PubMed, 42 citations in OpenAlex.
- RACK1 promotesiScience · 2023Article
- An Experimental Adult Zebrafish Model forMicrobiology spectrum · 2022Article
- NOD-Like Receptors: Guards of Cellular Homeostasis Perturbation during Infection.International journal of molecular sciences · 2021Review
- SIK2 orchestrates actin-dependent host response uponProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Shigella hijacks the exocyst to cluster macropinosomes for efficient vacuolar escape.PLoS pathogens · 2020Article
- Actin Assembly around the Shigella-Containing Vacuole Promotes Successful Infection.Cell reports · 2020Article
- SNX3 drives maturation ofThe Journal of cell biology · 2019Article
- Formate PromotesmBio · 2018Article
- Identification of Parameters of Host Cell Vulnerability during Salmonella Infection by Quantitative Image Analysis and Modeling.Infection and immunity · 2018Article
- Manipulation of host membranes by the bacterial pathogens Listeria, Francisella, Shigella and Yersinia.Seminars in cell & developmental biology · 2016Review
- Macropinosomes are Key Players in Early Shigella Invasion and Vacuolar Escape in Epithelial Cells.PLoS pathogens · 2016Article
- Cytosolic Access of Intracellular Bacterial Pathogens: The Shigella Paradigm.Frontiers in cellular and infection microbiology · 2016Review
- Bacterial Internalization, Localization, and Effectors Shape the Epithelial Immune Response during Shigella flexneri Infection.Infection and immunity · 2015Article
- Molecular mechanisms of host cytoskeletal rearrangements by Shigella invasins.International journal of molecular sciences · 2014Review
- Deciphering why Salmonella Gallinarum is less invasive in vitro than Salmonella Enteritidis.Veterinary research · 2014Article
- Maintenance of vacuole integrity by bacterial pathogens.Current opinion in microbiology · 2014Review
- The inside story of Shigella invasion of intestinal epithelial cells.Cold Spring Harbor perspectives in medicine · 2013Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shigella flexneri, the causative agent of bacillary dysentery, induces massive cytoskeletal rearrangement, resulting in its entry into nonphagocytic epithelial cells. The bacterium-engulfing membrane ruffles are formed by polymerizing actin, a process activated through injected bacterial effectors that target host small GTPases and tyrosine kinases. Once inside the host cell, S. flexneri escapes from the endocytic vacuole within minutes to move intra- and intercellularly. We quantified the fluorescence signals from fluorescently tagged host factors that are recruited to the site of pathogen entry and vacuolar escape. Quantitative time lapse fluorescence imaging revealed simultaneous recruitment of polymerizing actin, small GTPases of the Rho family, and tyrosine kinases. In contrast, we found that actin surrounding the vacuole containing bacteria dispersed first from the disassembling membranes, whereas other host factors remained colocalized with the membrane remnants. Furthermore, we found that the disassembly of the membrane remnants took place rapidly, within minutes after bacterial release into the cytoplasm. Superresolution visualization of galectin 3 through photoactivated localization microscopy characterized these remnants as small, specular, patchy structures between 30 and 300 nm in diameter. Using our experimental setup to track the time course of infection, we identified the S. flexneri effector IpgB1 as an accelerator of the infection pace, specifically targeting the entry step, but not vacuolar progression or escape. Together, our studies show that bacterial entry into host cells follows precise kinetics and that this time course can be targeted by the pathogen.
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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.