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dc.contributor.authorVan Dyck, K.en_US
dc.contributor.authorViela, F.en_US
dc.contributor.authorMathelié-Guinlet, M.en_US
dc.contributor.authorDemuyser, L.en_US
dc.contributor.authorHauben, E.en_US
dc.contributor.authorJabra-Rizk, M.A.en_US
dc.contributor.authorVande Velde, G.en_US
dc.contributor.authorDufrêne, Y.F.en_US
dc.contributor.authorKrom, B.P.en_US
dc.contributor.authorVan Dijck, P.en_US
dc.date.accessioned2021-04-12T16:48:47Z
dc.date.available2021-04-12T16:48:47Z
dc.date.issued2021-02-02
dc.identifier.urihttp://hdl.handle.net/10713/15232
dc.description.abstractInterspecies interactions greatly influence the virulence, drug tolerance and ultimately the outcome of polymicrobial biofilm infections. A synergistic interaction is observed between the fungus Candida albicans and the bacterium Staphylococcus aureus. These species are both normal commensals of most healthy humans and co-exist in several niches of the host. However, under certain circumstances, they can cause hospital-acquired infections with high morbidity and mortality rates. Using a mouse model of oral co-infection, we previously showed that an oral infection with C. albicans predisposes to a secondary systemic infection with S. aureus. Here, we unraveled this intriguing mechanism of bacterial dissemination. Using static and dynamic adhesion assays in combination with single-cell force spectroscopy, we identified C. albicans Als1 and Als3 adhesins as the molecular players involved in the interaction with S. aureus and in subsequent bacterial dissemination. Remarkably, we identified the host immune response as a key element required for bacterial dissemination. We found that the level of immunosuppression of the host plays a critical yet paradoxical role in this process. In addition, secretion of candidalysin, the C. albicans peptide responsible for immune activation and cell damage, is required for C. albicans colonization and subsequent bacterial dissemination. The physical interaction with C. albicans enhances bacterial uptake by phagocytic immune cells, thereby enabling an opportunity to disseminate. Copyright 2021 Van Dyck, Viela, Mathelié-Guinlet, Demuyser, Hauben, Jabra-Rizk, Vande Velde, Dufrêne, Krom and Van Dijck.en_US
dc.description.sponsorshipKV was supported by a personal research grant (1181818N) from the Fund for Scientific Research Flanders (FWO). This work was supported by the FWO research community on biofilms (W000921N) and by the National Institute of Allergy and Infectious Diseases of the NIH under award number R01AI130170 (NIAID) to MJ-R.en_US
dc.description.urihttps://doi.org/10.3389/fcimb.2020.624839en_US
dc.language.isoen_USen_US
dc.publisherFrontiers Media S.A.en_US
dc.relation.ispartofFrontiers in Cellular and Infection Microbiology
dc.subjectadhesinsen_US
dc.subjectCandida albicansen_US
dc.subjectcandidalysinen_US
dc.subjectimmune responseen_US
dc.subjectoral candidiasisen_US
dc.subjectpolymicrobialen_US
dc.subjectStaphylococcus aureusen_US
dc.titleAdhesion of Staphylococcus aureus to Candida albicans During Co-Infection Promotes Bacterial Dissemination Through the Host Immune Responseen_US
dc.typeArticleen_US
dc.identifier.doi10.3389/fcimb.2020.624839
dc.identifier.pmid33604309


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