Identification of a specific domain of Porphyromonas gingivalis Hgp44 responsible for adhesion to Treponema denticola

Identification of a specific domain of Porphyromonas gingivalis Hgp44 responsible for adhesion to... Abstract Interaction between two periodontal pathogens, Porphyromonas gingivalis and Treponema denticola, contributes to plaque biofilm formation. P. gingivalis forms aggregates with T. denticola through its adhesion/hemagglutinin domain (Hgp44). In this study, we investigated the specific domain of P. gingivalis Hgp44 responsible for adhesion to T. denticola using expression vectors harboring P. gingivalis Hgp44 DNA sequences encoding amino acid residues 1–419. Six plasmids harboring fragments in this region were generated by PCR amplification and self-ligation, and recombinant proteins r-Hgp44 (residues 1–419), r-Hgp441 (residues 1–124), r-Hgp442 (1–199), r-Hgp443 (1–316), r-Hgp444 (199–419), r-Hgp445 (124–198), and r-Hgp446 (199–316) were produced, as confirmed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis and immunoblotting. r-Hgp44, r-Hgp443, and r-Hgp446 showed greater adhesion to T. denticola sonicates than the control, as determined by enzyme-linked immunosorbent assay. r-Hgp446 reduced the coaggregation of P. gingivalis and T. denticola. scanning electron and confocal laser scanning microscopy analyses revealed that r-Hgp446 reduced dual-species biofilm formation. Our results indicate that residues 199–316 of P. gingivalis Hgp44 are mainly responsible for adhesion to T. denticola; inhibiting this domain could potentially disrupt periodontopathic biofilm formation and maturation. periodontitis, Porphyromonas gingivalis, Treponema denticola, coaggregation, adhesion, gingipain © FEMS 2018. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Pathogens and Disease Oxford University Press

Identification of a specific domain of Porphyromonas gingivalis Hgp44 responsible for adhesion to Treponema denticola

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Publisher
John Wiley & Sons Inc.
Copyright
© FEMS 2018.
ISSN
2049-632X
eISSN
2049-632X
D.O.I.
10.1093/femspd/fty047
Publisher site
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Abstract

Abstract Interaction between two periodontal pathogens, Porphyromonas gingivalis and Treponema denticola, contributes to plaque biofilm formation. P. gingivalis forms aggregates with T. denticola through its adhesion/hemagglutinin domain (Hgp44). In this study, we investigated the specific domain of P. gingivalis Hgp44 responsible for adhesion to T. denticola using expression vectors harboring P. gingivalis Hgp44 DNA sequences encoding amino acid residues 1–419. Six plasmids harboring fragments in this region were generated by PCR amplification and self-ligation, and recombinant proteins r-Hgp44 (residues 1–419), r-Hgp441 (residues 1–124), r-Hgp442 (1–199), r-Hgp443 (1–316), r-Hgp444 (199–419), r-Hgp445 (124–198), and r-Hgp446 (199–316) were produced, as confirmed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis and immunoblotting. r-Hgp44, r-Hgp443, and r-Hgp446 showed greater adhesion to T. denticola sonicates than the control, as determined by enzyme-linked immunosorbent assay. r-Hgp446 reduced the coaggregation of P. gingivalis and T. denticola. scanning electron and confocal laser scanning microscopy analyses revealed that r-Hgp446 reduced dual-species biofilm formation. Our results indicate that residues 199–316 of P. gingivalis Hgp44 are mainly responsible for adhesion to T. denticola; inhibiting this domain could potentially disrupt periodontopathic biofilm formation and maturation. periodontitis, Porphyromonas gingivalis, Treponema denticola, coaggregation, adhesion, gingipain © FEMS 2018. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/about_us/legal/notices)

Journal

Pathogens and DiseaseOxford University Press

Published: May 16, 2018

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