ArticleScientific reports2015
Adenylate Cyclase Toxin promotes bacterial internalisation into non phagocytic cells.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Mucosal IgA Antibodies are Critical for Bacterial Clearance ofPathogens & immunity · 2025Article
- Conquering the host:Frontiers in microbiology · 2022Review
- Hepcidin and Ferritin Predict Microbial Etiology in Community-Acquired Pneumonia.Open forum infectious diseases · 2021Article
- Susceptibility of Human Airway Tissue Models Derived From Different Anatomical Sites toFrontiers in cellular and infection microbiology · 2021Article
- Rck ofFrontiers in cellular and infection microbiology · 2020Article
- Functional and structural consequences of epithelial cell invasion by Bordetella pertussis adenylate cyclase toxin.PloS one · 2020Article
- Caveolae as Potential Hijackable Gates in Cell Communication.Frontiers in cell and developmental biology · 2020Review
- Bordetella Pertussis virulence factors in the continuing evolution of whooping cough vaccines for improved performance.Medical microbiology and immunology · 2018Review
- Bordetella Adenylate Cyclase-Hemolysin Toxins.Toxins · 2017Review
- Heterogeneous Family of Cyclomodulins: Smart Weapons That Allow Bacteria to Hijack the Eukaryotic Cell Cycle and Promote Infections.Frontiers in cellular and infection microbiology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bordetella pertussis causes whooping cough, a respiratory infectious disease that is the fifth largest cause of vaccine-preventable death in infants. Though historically considered an extracellular pathogen, this bacterium has been detected both in vitro and in vivo inside phagocytic and non-phagocytic cells. However the precise mechanism used by B. pertussis for cell entry, or the putative bacterial factors involved, are not fully elucidated. Here we find that adenylate cyclase toxin (ACT), one of the important toxins of B. pertussis, is sufficient to promote bacterial internalisation into non-phagocytic cells. After characterization of the entry route we show that uptake of "toxin-coated bacteria" proceeds via a clathrin-independent, caveolae-dependent entry pathway, allowing the internalised bacteria to survive within the cells. Intracellular bacteria were found inside non-acidic endosomes with high sphingomyelin and cholesterol content, or "free" in the cytosol of the invaded cells, suggesting that the ACT-induced bacterial uptake may not proceed through formation of late endolysosomes. Activation of Tyr kinases and toxin-induced Ca(2+)-influx are essential for the entry process. We hypothesize that B. pertussis might use ACT to activate the endocytic machinery of non-phagocytic cells and gain entry into these cells, in this way evading the host immune system.
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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.