Redistribution of the Novel Clostridioides difficile Spore Adherence Receptor E-Cadherin by TcdA and TcdB Increases Spore Binding to Adherens Junctions

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dc.contributor.authorCastro-Córdova, Pablo
dc.contributor.authorOtto-Medina, Macarena
dc.contributor.authorMontes-Bravo, Nicolás
dc.contributor.authorBrito-Silva, Christian
dc.contributor.authorLacy, D. Borden
dc.contributor.authorParedes-Sabja, Daniel
dc.date.accessioned2025-03-14T14:25:12Z
dc.date.available2025-03-14T14:25:12Z
dc.date.issued2023
dc.descriptionIndexación: Scopus
dc.description.abstractClostridioides difficile causes antibiotic-associated diseases in humans, ranging from mild diarrhea to severe pseudomembranous colitis and death. A major clinical challenge is the prevention of disease recurrence, which affects nearly;20 to 30% of the patients with a primary C. difficile infection (CDI). During CDI, C. difficile forms metabolically dormant spores that are essential for recurrence of CDI (R-CDI). In prior studies, we have shown that C. difficile spores interact with intestinal epithelial cells (IECs), which contribute to R-CDI. However, this interaction remains poorly understood. Here, we provide evidence that C. difficile spores interact with E-cadherin, contributing to spore adherence and internalization into IECs. C. difficile toxins TcdA and TcdB lead to adherens junctions opening and increase spore adherence to IECs. Confocal micrographs demonstrate that C. difficile spores associate with accessible E-cadherin; spore-E-cadherin association increases upon TcdA and TcdB intoxication. The presence of anti-E-cadherin antibodies decreased spore adherence and entry into IECs. By enzyme-linked immunosorbent assay (ELISA), immunofluorescence, and immunogold labeling, we observed that E-cadherin binds to C. difficile spores, specifically to the hairlike projections of the spore, reducing spore adherence to IECs. Overall, these results expand our knowledge of how C. difficile spores bind to IECs by providing evidence that E-cadherin acts as a spore adherence receptor to IECs and by revealing how toxin-mediated damage affects spore interactions with IECs. Copyright © 2022 American Society for Microbiology. All Rights Reserved
dc.description.urihttps://journals.asm.org/doi/epdf/10.1128/iai.00476-22?src=getftr&utm_source=scopus&getft_integrator=scopus
dc.identifier.doi10.1128/iai.00476-22
dc.identifier.issn00199567
dc.identifier.urihttps://repositorio.unab.cl/handle/ria/63770
dc.language.isoen_US
dc.publisherInfection and Immunity, Volume 91, Issue 1 January 2023
dc.rights.licenseAttribution 4.0 International CC BY 4.0 Deed
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectAdherens Junctions
dc.subjectBacterial Proteins
dc.subjectBacterial Toxins
dc.subjectClostridioides
dc.subjectClostridioides difficile
dc.subjectHumans
dc.subjectSpores, Bacterial
dc.subjectbacterial toxin
dc.subjectblocking antibody
dc.subjecttcda protein
dc.subjecttcdb protein
dc.subjectunclassified drug
dc.subjectuvomorulin
dc.subjectbacterial protein
dc.subjectbacterial toxin
dc.titleRedistribution of the Novel Clostridioides difficile Spore Adherence Receptor E-Cadherin by TcdA and TcdB Increases Spore Binding to Adherens Junctions
dc.typeArtículo
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