Journal of dentistry · 2020
Zinc chloride inhibits lysine decarboxylase production from Eikenella corrodens in vitro and its therapeutic implications.
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Levine Martin, Collins Lindsay M, Lohinai Zsolt
Аннотация
OBJECTIVES: Dentifrices containing zinc reduce gingival inflammation and bleeding better than control dentifrices (no zinc). How zinc might work is not understood. We have shown that lysine decarboxylase (LdcE), an enzyme from Eikenella corrodens, converts lysine to cadaverine in dental biofilms. The lack of lysine impairs the dentally attached cell barrier to biofilm, causing biofilm products to leak into junctional epithelium and stimulate inflammation. In year-old beagle dogs, immunization with LdcE, induces antibodies that inhibit LdcE activity and retard gingivitis development. We therefore examined whether a zinc-mediated loss of LdcE activity could explain the beneficial effect of zinc dentifrices.
METHODS: We grew E. corrodens in modified tryptic soy broth with or without zinc chloride, and extracted LdcE from the cell surface using a Potter Elvehjem homogenizer.
RESULTS: Up to 0.96 mM zinc chloride in the bacterial growth medium did not change cell yield, but reduced the extracted protein content by 41% (R2 = 0.27, p < 0.05) and LdcE activity/mg extracted protein by 85% (R2 = 0.90, p < 0.001). In extracts from cells grown without zinc, 78 times this zinc chloride concentration (73 mM) was required to reduce LdcE activity by 75%.
CONCLUSIONS: Zinc ions inhibit the production of protein with LdcE activity at E. corrodens cell surfaces. The zinc ions may attach to cysteine residues that are unique to the N-terminal region of LdcE by interfering with the non-covalent polypeptide assembly that produces enzyme activity.
CLINICAL SIGNIFICANCE: Zinc ion-mediated inhibition of LdcE assembly may provide a rationale for the improved control of gingival inflammation by zinc dentifrices.
METHODS: We grew E. corrodens in modified tryptic soy broth with or without zinc chloride, and extracted LdcE from the cell surface using a Potter Elvehjem homogenizer.
RESULTS: Up to 0.96 mM zinc chloride in the bacterial growth medium did not change cell yield, but reduced the extracted protein content by 41% (R2 = 0.27, p < 0.05) and LdcE activity/mg extracted protein by 85% (R2 = 0.90, p < 0.001). In extracts from cells grown without zinc, 78 times this zinc chloride concentration (73 mM) was required to reduce LdcE activity by 75%.
CONCLUSIONS: Zinc ions inhibit the production of protein with LdcE activity at E. corrodens cell surfaces. The zinc ions may attach to cysteine residues that are unique to the N-terminal region of LdcE by interfering with the non-covalent polypeptide assembly that produces enzyme activity.
CLINICAL SIGNIFICANCE: Zinc ion-mediated inhibition of LdcE assembly may provide a rationale for the improved control of gingival inflammation by zinc dentifrices.