Journal
MICROBIOLOGY-SGM
Volume 161, Issue -, Pages 168-181Publisher
MICROBIOLOGY SOC
DOI: 10.1099/mic.0.083485-0
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Funding
- National Institute of Allergy and Infectious Diseases, National Institutes of Health [R01AI69568]
- National Institute of Dental and Craniofacial Research, National Institutes of Health [1R01DE20939]
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007540, R01AI069568] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE020939, R01DE017088] Funding Source: NIH RePORTER
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Candida albicans and Staphylococcus aureus are often co-isolated in cases of biofilm-associated infections. C. albicans can cause systemic disease through morphological switch from the rounded yeast to the invasive hyphal form. Alternatively, systemic S. aureus infections arise from seeding through breaks in host epithelial layers although many patients have no documented portal of entry. We describe a novel strategy by which S. aureus is able to invade host tissue and disseminate via adherence to the invasive hyphal elements of Candida albicans. In vitro and ex vivo findings demonstrate a specific binding of the staphylococci to the candida hyphal elements. The C. albicans cell wall adhesin Als3p binds to multiple staphylococcal adhesins. Furthermore, Als3p is required for C. albicans to transport S. aureus into the tissue and cause a disseminated infection in an oral co-colonization model. These findings suggest that C. albicans can facilitate the invasion of S. aureus across mucosal barriers, leading to systemic infection in co-colonized patients.
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