Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in context
Summary: Background: Lifestyle- and sucrose-dependent polymicrobial ecological shifts are a primary cause of caries in populations with high caries prevalence. In populations with low prevalence, PRH1, PRH2 susceptibility and resistance phenotypes may interact with the Streptococcus mutans adhesin...
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| Format: | Article |
| Language: | English |
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Elsevier
2024-03-01
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| Series: | EBioMedicine |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2352396424000367 |
| _version_ | 1797305231544942592 |
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| author | Nongfei Sheng Lena Mårell Raviprakash Tumkur Sitaram Gunnel Svensäter Anna Westerlund Nicklas Strömberg |
| author_facet | Nongfei Sheng Lena Mårell Raviprakash Tumkur Sitaram Gunnel Svensäter Anna Westerlund Nicklas Strömberg |
| author_sort | Nongfei Sheng |
| collection | DOAJ |
| description | Summary: Background: Lifestyle- and sucrose-dependent polymicrobial ecological shifts are a primary cause of caries in populations with high caries prevalence. In populations with low prevalence, PRH1, PRH2 susceptibility and resistance phenotypes may interact with the Streptococcus mutans adhesin cariogenicity phenotype to affect caries progression, but studies are lacking on how these factors affect the microbial profile of caries. Methods: We analysed how the residency and infection profiles of S. mutans adhesin (SpaP A/B/C and Cnm/Cbm) phenotypes and commensal streptococci and lactobacilli influenced caries progression in a prospective case–referent sample of 452 Swedish adolescents with high (P4a), moderate (P6), and low (P1) caries PRH1, PRH2 phenotypes. Isolates of S. mutans from participants were analysed for adhesin expression and glycosylation and in vitro and in situ mechanisms related to caries activity. Findings: Among adolescents with the resistant (P1) phenotype, infection with S. mutans high-virulence phenotypes was required for caries progression. In contrast, with highly (P4a) or moderately (P6) susceptible phenotypes, caries developed from a broader polymicrobial flora that included moderately cariogenic oral commensal streptococci and lactobacilli and S. mutans phenotypes. High virulence involved unstable residency and fluctuating SpaP ABC, B-1, or Cnm expression/glycosylation phenotypes, whereas low/moderate virulence involved SpaP A phenotypes with stable residency. Adhesin phenotypes did not display changes in individual host residency but were paired within individuals and geographic regions. Interpretation: These results suggest that receptor PRH1, PRH2 susceptibility and resistance and S. mutans adhesin virulence phenotypes specify different microbial profiles in caries. Funding: Swedish Research Council and funding bodies listed in the acknowledgement section. |
| first_indexed | 2024-03-08T00:22:56Z |
| format | Article |
| id | doaj.art-73962b418be049f298458bcdd0ac1304 |
| institution | Directory Open Access Journal |
| issn | 2352-3964 |
| language | English |
| last_indexed | 2024-03-08T00:22:56Z |
| publishDate | 2024-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | EBioMedicine |
| spelling | doaj.art-73962b418be049f298458bcdd0ac13042024-02-16T04:29:15ZengElsevierEBioMedicine2352-39642024-03-01101105001Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in contextNongfei Sheng0Lena Mårell1Raviprakash Tumkur Sitaram2Gunnel Svensäter3Anna Westerlund4Nicklas Strömberg5Department of Odontology/Cariology, Umeå University, 901 87, Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, 901 87, Umeå, SwedenDepartment of Odontology/Cariology, Umeå University, 901 87, Umeå, SwedenFaculty of Odontology, Malmö University, 205 06, Malmö, SwedenDepartment of Orthodontics, Sahlgrenska Academy, University of Gothenburg, 413 90, Göteborg, SwedenDepartment of Odontology/Cariology, Umeå University, 901 87, Umeå, Sweden; Corresponding author. Department of Odontology/Cariology, Umeå University, SE-901 87, Umeå, Sweden.Summary: Background: Lifestyle- and sucrose-dependent polymicrobial ecological shifts are a primary cause of caries in populations with high caries prevalence. In populations with low prevalence, PRH1, PRH2 susceptibility and resistance phenotypes may interact with the Streptococcus mutans adhesin cariogenicity phenotype to affect caries progression, but studies are lacking on how these factors affect the microbial profile of caries. Methods: We analysed how the residency and infection profiles of S. mutans adhesin (SpaP A/B/C and Cnm/Cbm) phenotypes and commensal streptococci and lactobacilli influenced caries progression in a prospective case–referent sample of 452 Swedish adolescents with high (P4a), moderate (P6), and low (P1) caries PRH1, PRH2 phenotypes. Isolates of S. mutans from participants were analysed for adhesin expression and glycosylation and in vitro and in situ mechanisms related to caries activity. Findings: Among adolescents with the resistant (P1) phenotype, infection with S. mutans high-virulence phenotypes was required for caries progression. In contrast, with highly (P4a) or moderately (P6) susceptible phenotypes, caries developed from a broader polymicrobial flora that included moderately cariogenic oral commensal streptococci and lactobacilli and S. mutans phenotypes. High virulence involved unstable residency and fluctuating SpaP ABC, B-1, or Cnm expression/glycosylation phenotypes, whereas low/moderate virulence involved SpaP A phenotypes with stable residency. Adhesin phenotypes did not display changes in individual host residency but were paired within individuals and geographic regions. Interpretation: These results suggest that receptor PRH1, PRH2 susceptibility and resistance and S. mutans adhesin virulence phenotypes specify different microbial profiles in caries. Funding: Swedish Research Council and funding bodies listed in the acknowledgement section.http://www.sciencedirect.com/science/article/pii/S2352396424000367Streptococcus mutansHost susceptibilityPRH1/PRH2CariesCommensal pathogenAdhesion |
| spellingShingle | Nongfei Sheng Lena Mårell Raviprakash Tumkur Sitaram Gunnel Svensäter Anna Westerlund Nicklas Strömberg Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in context EBioMedicine Streptococcus mutans Host susceptibility PRH1/PRH2 Caries Commensal pathogen Adhesion |
| title | Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in context |
| title_full | Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in context |
| title_fullStr | Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in context |
| title_full_unstemmed | Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in context |
| title_short | Human PRH1, PRH2 susceptibility and resistance and Streptococcus mutans virulence phenotypes specify different microbial profiles in cariesResearch in context |
| title_sort | human prh1 prh2 susceptibility and resistance and streptococcus mutans virulence phenotypes specify different microbial profiles in cariesresearch in context |
| topic | Streptococcus mutans Host susceptibility PRH1/PRH2 Caries Commensal pathogen Adhesion |
| url | http://www.sciencedirect.com/science/article/pii/S2352396424000367 |
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