Role of sortase in Streptococcus mutans under the effect of nicotine.
- Author:
Ming-Yun LI
1
;
Rui-Jie HUANG
;
Xue-Dong ZHOU
;
Richard L GREGORY
Author Information
- Publication Type:Journal Article
- MeSH: Amino Acid Motifs; Aminoacyltransferases; drug effects; genetics; Antigens, Bacterial; drug effects; Bacterial Adhesion; drug effects; Bacterial Proteins; drug effects; genetics; Biofilms; drug effects; Cysteine Endopeptidases; drug effects; genetics; Dose-Response Relationship, Drug; Humans; Mutation; genetics; Nicotine; administration & dosage; pharmacology; Peptidoglycan; drug effects; genetics; Saliva; physiology; Streptococcus mutans; drug effects; enzymology; growth & development; Sucrose; pharmacology
- From: International Journal of Oral Science 2013;5(4):206-211
- CountryChina
- Language:English
- Abstract: Streptococcus mutans is a common Gram-positive bacterium and plays a significant role in dental caries. Tobacco and/or nicotine have documented effects on S. mutans growth and colonization. Sortase A is used by many Gram-positive bacteria, including S. mutans, to facilitate the insertion of certain cell surface proteins, containing an LPXTGX motif such as antigen I/II. This study examined the effect of nicotine on the function of sortase A to control the physiology and growth of S. mutans using wild-type S. mutans NG8, and its isogenic sortase-defective and -complemented strains. Briefly, the strains were treated with increasing amounts of nicotine in planktonic growth, biofilm metabolism, and sucrose-induced and saliva-induced antigen I/II-dependent biofilm formation assays. The strains exhibited no significant differences with different concentrations of nicotine in planktonic growth assays. However, they had significantly increased (P≤0.05) biofilm metabolic activity (2- to 3-fold increase) as the concentration of nicotine increased. Furthermore, the sortase-defective strain was more sensitive metabolically to nicotine than the wild-type or sortase-complemented strains. All strains had significantly increased sucrose-induced biofilm formation (2- to 3-fold increase) as a result of increasing concentrations of nicotine. However, the sortase-defective strain was not able to make as much sucrose- and saliva-induced biofilm as the wild-type NG8 did with increasing nicotine concentrations. These results indicated that nicotine increased metabolic activity and sucrose-induced biofilm formation. The saliva-induced biofilm formation assay and qPCR data suggested that antigen I/II was upregulated with nicotine but biofilm was not able to be formed as much as wild-type NG8 without functional sortase A.
