ArticleThe Journal of biological chemistry2010
Selective translocation of the Bordetella pertussis adenylate cyclase toxin across the basolateral membranes of polarized epithelial cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 46 citations in OpenAlex.
- Membrane-resolved epithelial electrophysiology revealed using extracellular electrochemical impedance spectroscopy (EEIS).bioRxiv : the preprint server for biology · 2026Article
- In Vitro Models for Investigating Intestinal Host-Pathogen Interactions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Early Circulating Edema Factor in Inhalational Anthrax Infection: Does It Matter?Microorganisms · 2024Article
- Article
- Bacterial Nucleotidyl Cyclases Activated by Calmodulin or Actin in Host Cells: Enzyme Specificities and Cytotoxicity Mechanisms Identified to Date.International journal of molecular sciences · 2022Review
- Article
- Suppression of mucosal Th17 memory responses by acellular pertussis vaccines enhances nasal Bordetella pertussis carriage.NPJ vaccines · 2021Article
- Susceptibility of Human Airway Tissue Models Derived From Different Anatomical Sites toFrontiers in cellular and infection microbiology · 2021Article
- Susceptibility of primary human airway epithelial cells toInnate immunity · 2021Article
- Functional and structural consequences of epithelial cell invasion by Bordetella pertussis adenylate cyclase toxin.PloS one · 2020Article
- Review
- Residues 529 to 549 participate in membrane penetration and pore-forming activity of the Bordetella adenylate cyclase toxin.Scientific reports · 2019Article
- Role of Major Toxin Virulence Factors in Pertussis Infection and Disease Pathogenesis.Advances in experimental medicine and biology · 2019Article
- Article
- Bordetella pertussis Adenylate Cyclase Toxin Disrupts Functional Integrity of Bronchial Epithelial Layers.Infection and immunity · 2018Article
- The conserved tyrosine residue 940 plays a key structural role in membrane interaction of Bordetella adenylate cyclase toxin.Scientific reports · 2017Article
- Cyclic AMP-Elevating Capacity of Adenylate Cyclase Toxin-Hemolysin Is Sufficient for Lung Infection but Not for Full Virulence of Bordetella pertussis.Infection and immunity · 2017Article
- Stability, structural and functional properties of a monomeric, calcium-loaded adenylate cyclase toxin, CyaA, from Bordetella pertussis.Scientific reports · 2017Article
- 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
- Bordetella adenylate cyclase toxin interacts with filamentous haemagglutinin to inhibit biofilm formation in vitro.Molecular microbiology · 2017Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
Abstract
The catalytic domain of Bordetella pertussis adenylate cyclase toxin (ACT) translocates directly across the plasma membrane of mammalian cells to induce toxicity by the production of cAMP. Here, we use electrophysiology to examine the translocation of toxin into polarized epithelial cells that model the mucosal surfaces of the host. We find that both polarized T84 cell monolayers and human airway epithelial cultures respond to nanomolar concentrations of ACT when applied to basolateral membranes, with little or no response to toxin applied apically. The induction of toxicity is rapid and fully explained by increases in intracellular cAMP, consistent with toxin translocation directly across the basolateral membrane. Intoxication of T84 cells occurs in the absence of CD11b/CD18 or evidence of another specific membrane receptor, and it is not dependent on post-translational acylation of the toxin or on host cell membrane potential, both previously reported to be required for toxin action. Thus, elements of the basolateral membrane render epithelial cells highly sensitive to the entry of ACT in the absence of a specific receptor for toxin binding.
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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.