ReviewFrontiers in cellular and infection microbiology2016
Molecular and Cellular Mechanisms of Shigella flexneri Dissemination.
Review in Frontiers in cellular and infection microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Article
- Sequential invasion of epithelial and immune cells in Shigellosis.bioRxiv : the preprint server for biology · 2026Article
- Lithocholic acid induces T3SS-dependent formation of invasion-competentInfection and immunity · 2026Article
- Article
- Genomic insights into Shigella species isolated from small ruminants and manure in the North West Province, South Africa.Applied microbiology and biotechnology · 2025Article
- Post-translational weapons of microbial warfare: how bacterial effectors hijack host cell death and xenophagy.Cell communication and signaling : CCS · 2025Review
- Can Nature Overcome Invasive Gastrointestinal Infections?International journal of molecular sciences · 2025Review
- Host PIK3C3 promotes Shigella flexneri spread from cell to cell through vacuole formation.PLoS pathogens · 2025Article
- Development of a visual Adhesion/Invasion Inhibition Assay to assess the functionality ofFrontiers in immunology · 2024Article
- RACK1 promotesiScience · 2023Article
- Review
- Molecular Mechanisms ofInternational journal of molecular sciences · 2023Review
- Pathogenicity and virulence ofVirulence · 2022Review
- A Shigella sonnei clone with extensive drug resistance associated with waterborne outbreaks in China.Nature communications · 2022Article
- Invading Bacterial Pathogens Activate Transcription Factor EB in Epithelial Cells through the Amino Acid Starvation Pathway of mTORC1 Inhibition.Molecular and cellular biology · 2022Article
- ThemBio · 2022Article
- The type three secretion system effector protein IpgB1 promotes Shigella flexneri cell-to-cell spread through double-membrane vacuole escape.PLoS pathogens · 2022Article
- The type 3 secretion effector IpgD promotes S. flexneri dissemination.PLoS pathogens · 2022Article
- The GBP1 microcapsule interferes with IcsA-dependent septin cage assembly around Shigella flexneri.Pathogens and disease · 2021Article
- TheMicroorganisms · 2021Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The intracellular pathogen Shigella flexneri is the causative agent of bacillary dysentery in humans. The disease is characterized by bacterial invasion of intestinal cells, dissemination within the colonic epithelium through direct spread from cell to cell, and massive inflammation of the intestinal mucosa. Here, we review the mechanisms supporting S. flexneri dissemination. The dissemination process primarily relies on actin assembly at the bacterial pole, which propels the pathogen throughout the cytosol of primary infected cells. Polar actin assembly is supported by polar expression of the bacterial autotransporter family member IcsA, which recruits the N-WASP/ARP2/3 actin assembly machinery. As motile bacteria encounter cell-cell contacts, they form plasma membrane protrusions that project into adjacent cells. In addition to the ARP2/3-dependent actin assembly machinery, protrusion formation relies on formins and myosins. The resolution of protrusions into vacuoles occurs through the collapse of the protrusion neck, leading to the formation of an intermediate membrane-bound compartment termed vacuole-like protrusions (VLPs). VLP formation requires tyrosine kinase and phosphoinositide signaling in protrusions, which relies on the integrity of the bacterial type 3 secretion system (T3SS). The T3SS is also required for escaping double membrane vacuoles through the activity of the T3SS translocases IpaB and IpaC, and the effector proteins VirA and IcsB. Numerous factors supporting envelope biogenesis contribute to IcsA exposure and maintenance at the bacterial pole, including LPS synthesis, membrane proteases, and periplasmic chaperones. Although less characterized, the assembly and function of the T3SS in the context of bacterial dissemination also relies on factors supporting envelope biogenesis. Finally, the dissemination process requires the adaptation of the pathogen to various cellular compartments through transcriptional and post-transcriptional mechanisms.
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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.