The road less traveled – defining molecular commensalism with <i>Streptococcus sanguinis</i>
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- J. Kreth
- Department of Restorative Dentistry Oregon Health and Science University Portland OR USA
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- R.A. Giacaman
- Cariology Unit Department of Oral Rehabilitation and Interdisciplinary Excellence Research Program on Healthy Aging (PIEI‐ES) University of Talca Talca Chile
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- R. Raghavan
- Department of Biology and Center for Life in Extreme Environments Portland State University Portland OR USA
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- J. Merritt
- Department of Restorative Dentistry Oregon Health and Science University Portland OR USA
説明
<jats:title>Summary</jats:title><jats:p>The commensal oral microbial flora has evolved with the human host to support colonization of the various intraoral sites without triggering a significant immune response. In exchange, the commensal microbes provide critical protection against invading pathogens. The intrinsic ability of the oral flora to create a symbiotic microbial community with the host can be disturbed, selecting for the overgrowth of a dysbiotic community that can result in dental diseases, such as caries and periodontitis. Although the mechanisms of molecular pathogenesis in oral diseases are well characterized, much less is known about the molecular mechanisms used by the commensal flora to maintain oral health. Here we focus on the commensal species <jats:italic>Streptococcus sanguinis</jats:italic>, which is found in abundance in the early oral biofilm and is strongly correlated with oral health. <jats:italic>Streptococcus sanguinis</jats:italic> exhibits a variety of features that make it ideally suited as a model organism to explore the molecular basis for commensalism. As such, this review will describe our current mechanistic understanding of <jats:italic>S. sanguinis</jats:italic> commensalism and speculate upon its molecular traits that may be exploitable to maintain or restore oral health under conditions that would otherwise lead to disease.</jats:p>
収録刊行物
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- Molecular Oral Microbiology
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Molecular Oral Microbiology 32 (3), 181-196, 2016-09-20
Wiley