Adhesion of Staphylococcus aureus to Candida albicans During Co-Infection Promotes Bacterial Dissemination Through the Host Immune Response

Frontiers in Cellular and Infection Microbiology

Greetje Vande Velde¹  Mary Ann Jabra-Rizk²  Bastiaan P. Krom³  Esther Hauben⁴  Katrien Van Dyck⁵  Liesbeth Demuyser⁵  Patrick Van Dijck⁵  Marion Mathelié-Guinlet⁶  Yves F. Dufrêne⁶  Felipe Viela⁶ 

[1] Biomedical MRI/MoSAIC, Department of Imaging and Pathology, KU Leuven, Leuven, Belgium;Department of Oncology and Diagnostic Sciences, Dental School, University of Maryland, Baltimore, Baltimore, MD, United States;Department of Microbiology and Immunology, School of Medicine, University of Maryland, Baltimore, Baltimore, MD, United States;Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), Vrije Universiteit Amsterdam and the University of Amsterdam, Amsterdam, Netherlands;Laboratory for Pathology, UZ Leuven and Department of Imaging and Pathology, Translational Cell and Tissue Research, KU Leuven, Leuven, Belgium;Laboratory of Molecular Cell Biology, Institute of Botany and Microbiology, Department of Biology, KU Leuven, Leuven, Belgium;VIB Center for Microbiology, Leuven, Belgium;Louvain Institute of Biomolecular Science and Technology (LIBST), UC Louvain, Louvain-la-Neuve, Belgium;

关键词: Candida albicans;    Staphylococcus aureus;    oral candidiasis;    polymicrobial;    adhesins;    immune response;    candidalysin;   

DOI  :  10.3389/fcimb.2020.624839

来源: Frontiers

【 摘 要 】

Interspecies 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.

【 授权许可】

CC BY