Biofilm lysine decarboxylase, a new therapeutic target for periodontal inflammation

Zsolt Lohinai, Beata Keremi, Eva Szöko, Tamás Tábi, Csaba Szabo, Zsolt Tulassay, John C. DiCesare, Carole A. Davis, Lindsay M. Collins, Martin Levine

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background: Lysine, a nutritionally essential amino acid, enters the oral cavity in gingival crevicular fluid (GCF). Duringoral hygiene restriction (OHR), lysine decarboxylase (LDC) in dento-gingival biofilms converts lysine to cadaverine. Lysine depletion impairs the dental epithelial barrier to bacterial proinflammatory products. Antibodies to LDC from Eikenella corrodens (Ecor-LDC) inhibit LDC activity and retard gingival inflammation in beagle dogs. Whether E. corrodens is the major source of LDC in dental biofilms and whether the lysine analog tranexamic acid (TA) inhibits LDC activity, biofilm accumulation, and GCF exudation in a human gingivitis model were examined. Methods: Antibodies raised in goats to LDC-rich extracts from E. corrodens cell surfaces were used to inhibit Ecor- LDC and detect it in biofilm extracts using Western blots. Ecor-LDC activity was measured at pH 4.0 to 11.0 and its TA dissociation constant (Ki) at pH 7.0. Young adults used a 5% or 10% TA mouthwash three times daily during OHR for 1 week. Results: Ecor-LDC antibodies and TA inhibited biofilm LDC. Ki of TA for Ecor-LDC was 940 μM. TA reduced plaque index (PI) by downshifting the PI correlation with biofilm lysine content after OHR without TA. GCF was correspondingly suppressed. However, greater TA retention in saliva partially relieved GCF suppression but not biofilm lysine depletion. Conclusions: TA slightly inhibits LDC but strongly reduces biofilm by inhibiting bacterial lysine uptake. Unfortunately, TA may impair dental epithelial attachments by also inhibiting lysine transporter uptake. Ecor-LDC inhibitors other than lysine analogs may maintain sufficient lysine levels and attachment integrity to prevent periodontal inflammation. J Periodontol 2015;86:1176-1184.

Original languageEnglish (US)
Pages (from-to)1176-1184
Number of pages9
JournalJournal of Periodontology
Volume86
Issue number10
DOIs
StatePublished - Oct 1 2015

Fingerprint

lysine decarboxylase
Biofilms
Tranexamic Acid
Inflammation
Lysine
Gingival Crevicular Fluid
Eikenella corrodens
Therapeutics
Tooth
Antibodies

Keywords

  • Biomarkers
  • Dental Plaque
  • Drug Delivery Systems
  • Gingival Crevicular Fluid
  • Gingivitis/oral hygiene
  • Pharmacological

ASJC Scopus subject areas

  • Periodontics

Cite this

Lohinai, Z., Keremi, B., Szöko, E., Tábi, T., Szabo, C., Tulassay, Z., ... Levine, M. (2015). Biofilm lysine decarboxylase, a new therapeutic target for periodontal inflammation. Journal of Periodontology, 86(10), 1176-1184. https://doi.org/10.1902/jop.2015.140490

Biofilm lysine decarboxylase, a new therapeutic target for periodontal inflammation. / Lohinai, Zsolt; Keremi, Beata; Szöko, Eva; Tábi, Tamás; Szabo, Csaba; Tulassay, Zsolt; DiCesare, John C.; Davis, Carole A.; Collins, Lindsay M.; Levine, Martin.

In: Journal of Periodontology, Vol. 86, No. 10, 01.10.2015, p. 1176-1184.

Research output: Contribution to journalArticle

Lohinai, Z, Keremi, B, Szöko, E, Tábi, T, Szabo, C, Tulassay, Z, DiCesare, JC, Davis, CA, Collins, LM & Levine, M 2015, 'Biofilm lysine decarboxylase, a new therapeutic target for periodontal inflammation', Journal of Periodontology, vol. 86, no. 10, pp. 1176-1184. https://doi.org/10.1902/jop.2015.140490
Lohinai, Zsolt ; Keremi, Beata ; Szöko, Eva ; Tábi, Tamás ; Szabo, Csaba ; Tulassay, Zsolt ; DiCesare, John C. ; Davis, Carole A. ; Collins, Lindsay M. ; Levine, Martin. / Biofilm lysine decarboxylase, a new therapeutic target for periodontal inflammation. In: Journal of Periodontology. 2015 ; Vol. 86, No. 10. pp. 1176-1184.
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abstract = "Background: Lysine, a nutritionally essential amino acid, enters the oral cavity in gingival crevicular fluid (GCF). Duringoral hygiene restriction (OHR), lysine decarboxylase (LDC) in dento-gingival biofilms converts lysine to cadaverine. Lysine depletion impairs the dental epithelial barrier to bacterial proinflammatory products. Antibodies to LDC from Eikenella corrodens (Ecor-LDC) inhibit LDC activity and retard gingival inflammation in beagle dogs. Whether E. corrodens is the major source of LDC in dental biofilms and whether the lysine analog tranexamic acid (TA) inhibits LDC activity, biofilm accumulation, and GCF exudation in a human gingivitis model were examined. Methods: Antibodies raised in goats to LDC-rich extracts from E. corrodens cell surfaces were used to inhibit Ecor- LDC and detect it in biofilm extracts using Western blots. Ecor-LDC activity was measured at pH 4.0 to 11.0 and its TA dissociation constant (Ki) at pH 7.0. Young adults used a 5{\%} or 10{\%} TA mouthwash three times daily during OHR for 1 week. Results: Ecor-LDC antibodies and TA inhibited biofilm LDC. Ki of TA for Ecor-LDC was 940 μM. TA reduced plaque index (PI) by downshifting the PI correlation with biofilm lysine content after OHR without TA. GCF was correspondingly suppressed. However, greater TA retention in saliva partially relieved GCF suppression but not biofilm lysine depletion. Conclusions: TA slightly inhibits LDC but strongly reduces biofilm by inhibiting bacterial lysine uptake. Unfortunately, TA may impair dental epithelial attachments by also inhibiting lysine transporter uptake. Ecor-LDC inhibitors other than lysine analogs may maintain sufficient lysine levels and attachment integrity to prevent periodontal inflammation. J Periodontol 2015;86:1176-1184.",
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AU - Tábi, Tamás

AU - Szabo, Csaba

AU - Tulassay, Zsolt

AU - DiCesare, John C.

AU - Davis, Carole A.

AU - Collins, Lindsay M.

AU - Levine, Martin

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N2 - Background: Lysine, a nutritionally essential amino acid, enters the oral cavity in gingival crevicular fluid (GCF). Duringoral hygiene restriction (OHR), lysine decarboxylase (LDC) in dento-gingival biofilms converts lysine to cadaverine. Lysine depletion impairs the dental epithelial barrier to bacterial proinflammatory products. Antibodies to LDC from Eikenella corrodens (Ecor-LDC) inhibit LDC activity and retard gingival inflammation in beagle dogs. Whether E. corrodens is the major source of LDC in dental biofilms and whether the lysine analog tranexamic acid (TA) inhibits LDC activity, biofilm accumulation, and GCF exudation in a human gingivitis model were examined. Methods: Antibodies raised in goats to LDC-rich extracts from E. corrodens cell surfaces were used to inhibit Ecor- LDC and detect it in biofilm extracts using Western blots. Ecor-LDC activity was measured at pH 4.0 to 11.0 and its TA dissociation constant (Ki) at pH 7.0. Young adults used a 5% or 10% TA mouthwash three times daily during OHR for 1 week. Results: Ecor-LDC antibodies and TA inhibited biofilm LDC. Ki of TA for Ecor-LDC was 940 μM. TA reduced plaque index (PI) by downshifting the PI correlation with biofilm lysine content after OHR without TA. GCF was correspondingly suppressed. However, greater TA retention in saliva partially relieved GCF suppression but not biofilm lysine depletion. Conclusions: TA slightly inhibits LDC but strongly reduces biofilm by inhibiting bacterial lysine uptake. Unfortunately, TA may impair dental epithelial attachments by also inhibiting lysine transporter uptake. Ecor-LDC inhibitors other than lysine analogs may maintain sufficient lysine levels and attachment integrity to prevent periodontal inflammation. J Periodontol 2015;86:1176-1184.

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