ReviewOpen biology2013
Molecular mechanisms of cell-cell spread of intracellular bacterial pathogens.
Review in Open biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 66 citations in OpenAlex.
- Role of Flotillin-1 In Listeria monocytogenes Cell-to-Cell Spreading.The Journal of infectious diseases · 2025Article
- Deep sequencing of 16mSystems · 2025Article
- The host GTPase Dynamin 2 modulates apical junction structure to control cell-to-cell spread ofInfection and immunity · 2024Article
- In vitro characterization of Trypanosoma cruzi infection dynamics in skeletal and cardiac myotubes models suggests a potential cell-to-cell transmission in mediating cardiac pathology.PLoS neglected tropical diseases · 2024Article
- Spotted fever rickettsia-induced microvascular endothelial barrier dysfunction is delayed by the calcium channel blocker benidipine.Biochemical and biophysical research communications · 2023Article
- Review
- Function-based classification of hazardous biological sequences: Demonstration of a new paradigm for biohazard assessments.Frontiers in bioengineering and biotechnology · 2022Article
- Host Epigenetics in Intracellular Pathogen Infections.International journal of molecular sciences · 2020Review
- Article
- Article
- Pathogenic Puppetry: Manipulation of the Host Actin Cytoskeleton byInternational journal of molecular sciences · 2019Review
- Bacterial Synchronized Transfer Assays in Bone Marrow Derived Macrophages.Bio-protocol · 2019Article
- Counterattacking the tick bite: towards a rational design of anti-tick vaccines targeting pathogen transmission.Parasites & vectors · 2019Review
- Antigenic and functional profiles of a Lawsonia intracellularis protein that shows a flagellin-like trait and its immuno-stimulatory assessment.Veterinary research · 2018Article
- In vitro studies of Rickettsia-host cell interactions: Confocal laser scanning microscopy of Rickettsia helvetica-infected eukaryotic cell lines.PLoS neglected tropical diseases · 2018Article
- Article
- Extracellular motility and cell-to-cell transmission of enterohemorrhagic E. coli is driven by EspFU-mediated actin assembly.PLoS pathogens · 2017Article
- Actin-based motility and cell-to-cell spread of bacterial pathogens.Current opinion in microbiology · 2017Review
- Tick-Pathogen Interactions and Vector Competence: Identification of Molecular Drivers for Tick-Borne Diseases.Frontiers in cellular and infection microbiology · 2017Review
- Microbial Invasion vs. Tick Immune Regulation.Frontiers in cellular and infection microbiology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Several bacterial pathogens, including Listeria monocytogenes, Shigella flexneri and Rickettsia spp., have evolved mechanisms to actively spread within human tissues. Spreading is initiated by the pathogen-induced recruitment of host filamentous (F)-actin. F-actin forms a tail behind the microbe, propelling it through the cytoplasm. The motile pathogen then encounters the host plasma membrane, forming a bacterium-containing protrusion that is engulfed by an adjacent cell. Over the past two decades, much progress has been made in elucidating mechanisms of F-actin tail formation. Listeria and Shigella produce tails of branched actin filaments by subverting the host Arp2/3 complex. By contrast, Rickettsia forms tails with linear actin filaments through a bacterial mimic of eukaryotic formins. Compared with F-actin tail formation, mechanisms controlling bacterial protrusions are less well understood. However, recent findings have highlighted the importance of pathogen manipulation of host cell-cell junctions in spread. Listeria produces a soluble protein that enhances bacterial protrusions by perturbing tight junctions. Shigella protrusions are engulfed through a clathrin-mediated pathway at 'tricellular junctions'--specialized membrane regions at the intersection of three epithelial cells. This review summarizes key past findings in pathogen spread, and focuses on recent developments in actin-based motility and the formation and internalization of bacterial protrusions.
Indexed as
Identifiers
What OpenQuestion holds
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.