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Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation

BACKGROUND: Periodontitis is caused by a dysbiotic shift in the dental plaque microbiome. Fusobacterium nucleatum is involved in the colonization of Porphyromonas gingivalis, which plays a key role in dysbiosis, via coaggregation and synergy with this microorganism. AIM: We investigated the effect o...

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Autores principales: Yamaguchi-Kuroda, Yukiko, Kikuchi, Yuichiro, Kokubu, Eitoyo, Ishihara, Kazuyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9848294/
https://www.ncbi.nlm.nih.gov/pubmed/36687169
http://dx.doi.org/10.1080/20002297.2023.2165001
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author Yamaguchi-Kuroda, Yukiko
Kikuchi, Yuichiro
Kokubu, Eitoyo
Ishihara, Kazuyuki
author_facet Yamaguchi-Kuroda, Yukiko
Kikuchi, Yuichiro
Kokubu, Eitoyo
Ishihara, Kazuyuki
author_sort Yamaguchi-Kuroda, Yukiko
collection PubMed
description BACKGROUND: Periodontitis is caused by a dysbiotic shift in the dental plaque microbiome. Fusobacterium nucleatum is involved in the colonization of Porphyromonas gingivalis, which plays a key role in dysbiosis, via coaggregation and synergy with this microorganism. AIM: We investigated the effect of diffusible signaling molecules from P. gingivalis ATCC 33277 on F. nucleatum TDC 100 to elucidate the synergistic mechanisms involved in dysbiosis. METHODS: The two species were cocultured separated with an 0.4-µm membrane in tryptic soy broth, and F. nucleatum gene expression profiles in coculture with P. gingivalis were compared with those in monoculture. RESULTS: RNA sequencing revealed 139 genes differentially expressed between the coculture and monoculture. The expression of 52 genes was upregulated, including the coaggregation ligand-coding gene. Eighty-seven genes were downregulated. Gene Ontology analysis indicated enrichment for the glycogen synthesis pathway and a decrease in de novo synthesis of purine and pyrimidine. CONCLUSION: These results indicate that diffusible signaling molecules from P. gingivalis induce metabolic changes in F. nucleatum, including an increase in polysaccharide synthesis and reduction in de novo synthesis of purine and pyrimidine. The metabolic changes may accelerate biofilm formation by F. nucleatum with P. gingivalis. Further, the alterations may represent potential therapeutic targets for preventing dysbiosis.
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spelling pubmed-98482942023-01-19 Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation Yamaguchi-Kuroda, Yukiko Kikuchi, Yuichiro Kokubu, Eitoyo Ishihara, Kazuyuki J Oral Microbiol Original Article BACKGROUND: Periodontitis is caused by a dysbiotic shift in the dental plaque microbiome. Fusobacterium nucleatum is involved in the colonization of Porphyromonas gingivalis, which plays a key role in dysbiosis, via coaggregation and synergy with this microorganism. AIM: We investigated the effect of diffusible signaling molecules from P. gingivalis ATCC 33277 on F. nucleatum TDC 100 to elucidate the synergistic mechanisms involved in dysbiosis. METHODS: The two species were cocultured separated with an 0.4-µm membrane in tryptic soy broth, and F. nucleatum gene expression profiles in coculture with P. gingivalis were compared with those in monoculture. RESULTS: RNA sequencing revealed 139 genes differentially expressed between the coculture and monoculture. The expression of 52 genes was upregulated, including the coaggregation ligand-coding gene. Eighty-seven genes were downregulated. Gene Ontology analysis indicated enrichment for the glycogen synthesis pathway and a decrease in de novo synthesis of purine and pyrimidine. CONCLUSION: These results indicate that diffusible signaling molecules from P. gingivalis induce metabolic changes in F. nucleatum, including an increase in polysaccharide synthesis and reduction in de novo synthesis of purine and pyrimidine. The metabolic changes may accelerate biofilm formation by F. nucleatum with P. gingivalis. Further, the alterations may represent potential therapeutic targets for preventing dysbiosis. Taylor & Francis 2023-01-10 /pmc/articles/PMC9848294/ /pubmed/36687169 http://dx.doi.org/10.1080/20002297.2023.2165001 Text en © 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Yamaguchi-Kuroda, Yukiko
Kikuchi, Yuichiro
Kokubu, Eitoyo
Ishihara, Kazuyuki
Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation
title Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation
title_full Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation
title_fullStr Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation
title_full_unstemmed Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation
title_short Porphyromonas gingivalis diffusible signaling molecules enhance Fusobacterium nucleatum biofilm formation via gene expression modulation
title_sort porphyromonas gingivalis diffusible signaling molecules enhance fusobacterium nucleatum biofilm formation via gene expression modulation
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9848294/
https://www.ncbi.nlm.nih.gov/pubmed/36687169
http://dx.doi.org/10.1080/20002297.2023.2165001
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