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Microb Ecol. 2018 Nov 24. doi: 10.1007/s00248-018-1291-0. [Epub ahead of print]

The Oral Bacterium Fusobacterium nucleatum Binds Staphylococcus aureus and Alters Expression of the Staphylococcal Accessory Regulator sarA.

Author information

1
Division of Constitutive and Regenerative Sciences, School of Dentistry, University of California, Los Angeles, CA, USA.
2
Department of Diagnostic and Biological Sciences, School of Dentistry, Universit of Minnesota, Minneapolis, MN, USA.
3
Department of Biochemistry, University of Wisconsin-Madison, 440 Henry Mall, Madison, WI, USA.
4
Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
5
Department of Chemistry, University of Wisconsin-Madison, 440 Henry Mall, Madison, WI, USA.
6
Department of Biomedical Engineering, University of Wisconsin-Madison, 440 Henry Mall, Madison, WI, USA.
7
Division of Constitutive and Regenerative Sciences, School of Dentistry, University of California, Los Angeles, CA, USA. rlux@dentistry.ucla.edu.

Abstract

Staphylococcus aureus, an opportunistic pathogen member of the nasal and skin microbiota, can also be found in human oral samples and has been linked to infectious diseases of the oral cavity. As the nasal and oral cavities are anatomically connected, it is currently unclear whether S. aureus can colonize the oral cavity and become part of the oral microbiota, or if its presence in the oral cavity is simply transient. To start addressing this question, we assessed S. aureus ability to directly bind selected members of the oral microbiota as well as its ability to integrate into a human-derived complex oral microbial community in vitro. Our data show that S. aureus forms aggregates with Fusobacterium nucleatum and Porphyromonas gingivalis and that it can incorporate into the human-derived in vitro oral community. Further analysis of the F. nucleatum-S. aureus interaction revealed that the outer-membrane adhesin RadD is partially involved in aggregate formation and that the RadD-mediated interaction leads to an increase in expression of the staphylococcal global regulator gene sarA. Our findings lend support to the notion that S. aureus can become part of the complex microbiota of the human mouth, which could serve as a reservoir for S. aureus. Furthermore, direct interaction with key members of the oral microbiota could affect S. aureus pathogenicity contributing to the development of several S. aureus associated oral infections.

KEYWORDS:

Coaggregation; Fusobacterium; Oral ecology; SarA; Staphylococcus

PMID:
30474730
DOI:
10.1007/s00248-018-1291-0

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