Role of sortase in Streptococcus mutans under the effect of nicotine

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.

Effects of Nicotine on Streptococcus gordonii Growth, Biofilm Formation, and Cell Aggregation

“…Unlike abp-A, the abp-B mutant strain retains the ability to bind to soluble amylase (29). abp-A, instead of abp-B, is the major protein for S. gordonii tooth surface binding (33), and the present study confirmed that the expression of abp-A was much higher than that of abp-B (Fig. 3).…”

“…An SrtA mutant of S. gordonii demonstrated less biofilm and impaired binding ability (35). Previous studies in our laboratory demonstrated that sortase-defective S. mutans forms less biofilm than the wild type under the same nicotine treatment (33). The promotion effect of nicotine on S. gordonii srtA expression partially explains the increased biofilm formation in nicotine-treated groups.…”

The role of nicotine, cotinine and caffeine on the electrochemical behavior and bacterial colonization to cp-Ti

“…WD = 8 mm; 15 Kv. nicotine [48]. This might explain why S. sanguinis biofilm exposed to nicotine (0.3, 3 and 30 μg/mL) enhanced carbohydrate levels in our study.…”

Antimicrobial peptide GH12 suppresses cariogenic virulence factors of Streptococcus mutans

“…Each PCR reagent (25 μL) contained SYBR® Premix Ex Taq ™ II (RR820A; Takara Bio), cDNA samples (80 ng) and forward and reverse gene-specific primers (10 μM, 1 μL each). The qPCR was performed on CFX96 Real-Time System (C1000™ Thermal Cycler; Bio-Rad, Hercules, CA) using the same thermocycling conditions as in a previous study [35]. The 2 −ΔΔCt method was used to calculate gene expression fold change, and different gene expressions were normalized to the levels of 16S rRNA gene transcripts.…”