한빛사논문
- 조회238
Hunyong Cho 1,13, Zhi Ren 2,13, Kimon Divaris 3,4, Jeffrey Roach 5,6, Bridget M. Lin 1, Chuwen Liu 1, M. Andrea Azcarate-Peril 6,7, Miguel A. Simancas-Pallares 3, Poojan Shrestha 3,4, Alena Orlenko 8, Jeannie Ginnis 3, Kari E. North 4, Andrea G. Ferreira Zandona 9, Apoena Aguiar Ribeiro 10, Di Wu 1,11 & Hyun Koo 2,12
1Department of Biostatistics, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
2Biofilm Research Laboratories, Center for Innovation & Precision Dentistry, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.
3Division of Pediatric and Public Health, Adams School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
4Department of Epidemiology, Gillings School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
5UNC Information Technology Services and Research Computing, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
6UNC Microbiome Core, Center for Gastrointestinal Biology and Disease, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
7Department of Medicine, Division of Gastroenterology and Hepatology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
8Artificial Intelligence Innovation Lab, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
9Department of Comprehensive Care, School of Dental Medicine, Tufts University, Boston, MA, USA.
10Division of Diagnostic Sciences, Adams School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
11Division of Oral and Craniofacial Health Sciences, Adams School of Dentistry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
12Department of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA, USA.
These authors contributed equally: Hunyong Cho, Zhi Ren.
Corresponding author: correspondence to Kimon Divaris, Di Wu or Hyun Koo
Abstract
Streptococcus mutans has been implicated as the primary pathogen in childhood caries (tooth decay). While the role of polymicrobial communities is appreciated, it remains unclear whether other microorganisms are active contributors or interact with pathogens. Here, we integrate multi-omics of supragingival biofilm (dental plaque) from 416 preschool-age children (208 males and 208 females) in a discovery-validation pipeline to identify disease-relevant inter-species interactions. Sixteen taxa associate with childhood caries in metagenomics-metatranscriptomics analyses. Using multiscale/computational imaging and virulence assays, we examine biofilm formation dynamics, spatial arrangement, and metabolic activity of Selenomonas sputigena, Prevotella salivae and Leptotrichia wadei, either individually or with S. mutans. We show that S. sputigena, a flagellated anaerobe with previously unknown role in supragingival biofilm, becomes trapped in streptococcal exoglucans, loses motility but actively proliferates to build a honeycomb-like multicellular-superstructure encapsulating S. mutans, enhancing acidogenesis. Rodent model experiments reveal an unrecognized ability of S. sputigena to colonize supragingival tooth surfaces. While incapable of causing caries on its own, when co-infected with S. mutans, S. sputigena causes extensive tooth enamel lesions and exacerbates disease severity in vivo. In summary, we discover a pathobiont cooperating with a known pathogen to build a unique spatial structure and heighten biofilm virulence in a prevalent human disease.
논문정보
- Research article
- 2023년 05월 (BRIC 등록일 2023-06-02)
- 국외 연구진
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