ArticlePLoS pathogens2017
Pseudomonas aeruginosa ExlA and Serratia marcescens ShlA trigger cadherin cleavage by promoting calcium influx and ADAM10 activation.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Role of PsrA in physiology and virulence regulation inJournal of bacteriology · 2026Review
- A decade of insight into ExlA toxin research and the biotechnological potential of non-virulentJournal of bacteriology · 2026Review
- Hemolytic mechanism and virulence of Antarctic psychrophilicFrontiers in microbiology · 2026Article
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Cleavage of cell junction proteins as a host invasion strategy in leptospirosis.Applied microbiology and biotechnology · 2024Review
- Regulation of ADAM10 activity through microdomain-dependent intracellular calcium changes.Cell communication and signaling : CCS · 2024Article
- The Balance between Protealysin and Its Substrate, the Outer Membrane Protein OmpX, RegulatesInternational journal of molecular sciences · 2024Review
- G protein-coupled estrogen receptor agonist G-1 decreases ADAM10 levels and NLRP3-inflammasome component activation in response to Staphylococcus aureus alpha-hemolysin.MicrobiologyOpen · 2024Article
- Host-Cell-Dependent Roles of E-Cadherin inInternational journal of molecular sciences · 2023Article
- Endothelial ADAM10 utilization defines a molecular pathway of vascular injury in mice with bacterial sepsis.The Journal of clinical investigation · 2023Article
- The Anti-Virulence Activities of the Antihypertensive Drug Propranolol in Light of Its Anti-Quorum Sensing Effects againstBiomedicines · 2023Article
- Pore-forming activity ofInfection and immunity · 2023Article
- Current concepts on Pseudomonas aeruginosa interaction with human airway epithelium.PLoS pathogens · 2023Review
- ADAM10-a "multitasker" in sepsis: focus on its posttranslational target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Genomic erosion and horizontal gene transfer shape functional differences of the ExlA toxin iniScience · 2022Article
- Bacterial pore-forming toxins.Microbiology (Reading, England) · 2022Article
- Dynamic Python-Based Method Provides Quantitative Analysis of Intercellular Junction Organization DuringFrontiers in cellular and infection microbiology · 2022Article
- Alpha-1 antitrypsin limits neutrophil extracellular trap disruption of airway epithelial barrier function.Frontiers in immunology · 2022Article
- ExlA: A New Contributor toFrontiers in cellular and infection microbiology · 2022Review
- Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.Advances in experimental medicine and biology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pore-forming toxins are potent virulence factors secreted by a large array of bacteria. Here, we deciphered the action of ExlA from Pseudomonas aeruginosa and ShlA from Serratia marcescens on host cell-cell junctions. ExlA and ShlA are two members of a unique family of pore-forming toxins secreted by a two-component secretion system. Bacteria secreting either toxin induced an ExlA- or ShlA-dependent rapid cleavage of E-cadherin and VE-cadherin in epithelial and endothelial cells, respectively. Cadherin proteolysis was executed by ADAM10, a host cell transmembrane metalloprotease. ADAM10 activation is controlled in the host cell by cytosolic Ca2+ concentration. We show that Ca2+ influx, induced by ExlA or ShlA pore formation in the plasma membrane, triggered ADAM10 activation, thereby leading to cadherin cleavage. Our data suggest that ADAM10 is not a cellular receptor for ExlA and ShlA, further confirming that ADAM10 activation occurred via Ca2+ signalling. In conclusion, ExlA- and ShlA-secreting bacteria subvert a regulation mechanism of ADAM10 to activate cadherin shedding, inducing intercellular junction rupture, cell rounding and loss of tissue barrier integrity.
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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.