Adhesion of Staphylococcus aureus to Candida albicans During Co-Infection Promotes Bacterial Dissemination Through the Host Immune Response
AuthorVan Dyck, K.
Vande Velde, G.
Van Dijck, P.
JournalFrontiers in Cellular and Infection Microbiology
PublisherFrontiers Media S.A.
MetadataShow full item record
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.
SponsorsKV 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.
Identifier to cite or link to this itemhttp://hdl.handle.net/10713/15232
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