Abstract
Staphylococcus epidermidis is a common bacterial colonizer of human skin and mucous membranes, yet it has emerged as an important nosocomial pathogen largely due to its ability to form biofilms. Tobacco smoke has been demonstrated as a contributor to various infection diseases by improving the biofilm formation of multiple bacterial species; however, the association between tobacco smoke and S. epidermidis biofilm is still unclear. In this study, we tested the effect of nicotine, one of the most active components of tobacco, on S. epidermidis biofilm formation, and we studied the underlying mechanisms. Our results showed that nicotine promoted the biofilm formation of S. epidermidis 1457 strain (SE1457) and enhanced its initial attachment to a polyethylene surface as well as polysaccharide intercellular adhesin (PIA) production. In addition, an increased extracellular DNA release and a higher autolysis rate of SE1457 was detected after nicotine treatment, which was consistent with the increased ratio of dead cells in nicotine-treated SE1457 biofilm observed with confocal laser-scanning microscopy. Furthermore, the effect of nicotine on several autolysis-related and biofilm-related gene knockout mutants of SE1457 was tested. It showed that in ΔsaeRS, ΔlytSR, and ΔsceD, nicotine induced increase in biofilm formation was similar to that in SE1457; but in ΔarlRS, ΔatlE, and ΔicaC, the effect was obviously impaired. Consistently, the increase of the bacterial autolysis rate in ΔarlRS and ΔatlE induced by nicotine was not as significant as that in SE1457. Meanwhile, the growth inhibition of nicotine on SE1457 was observed, and it was much less on ΔarlRS and restored by the arlRS complementation. The arlRS transcription in SE1457 was inhibited by nicotine during cultivation as indicated by a promoter reporter assay using green fluoresent protein. Taken together, our study indicates that nicotine improves S. epidermidis biofilm formation by promoting its initial attachment and intercellular accumulation; the arlRS, atlE, and ica genes mediating bacterial autolysis and PIA production play an important role in this process.
Highlights
Staphylococcus epidermidis (S. epidermidis) is an oppotunistic pathogen that commonly colonizes on the human skin and mocosal surfaces
In order to determine the effects of nicotine on S. epidermidis biofilm formation, SE1457 strain was exposed to different concentrations of nicotine (0, 100, 200, 500, 1000, 2000, 4000, 8000, and 16000 μg/ml) for 24 h at 37◦C
We found that stimulation of S. epidermidis biofilm formation by nicotine was more obvious when the polyethylene plates were coated with human fibrinogen or when nicotine treatment was extended from 24 to 48 h, even if lower concentrations of nicotine were used (Supplementary Figures S1, S2)
Summary
Staphylococcus epidermidis (S. epidermidis) is an oppotunistic pathogen that commonly colonizes on the human skin and mocosal surfaces. Bacteria within biofilm are encased in self-produced matrix composed of extracellular polysaccharide, DNA, and proteins (Rabin et al, 2015). Given their high degree of resistance to the human immune system and current antimicrobial agents, bacterial biofilm plays an important role in the persistence of many chronic human infections (Parsek and Singh, 2003). Huang et al reported that nicotine could stimulate Streptococcus mutans biofilm formation and its metabolic activity (Huang et al, 2012; Li et al, 2014; Huang et al, 2015) They found that nicotine could enhance Streptococcus gordonii biofilm formation, aggregation, and gene expression of binding proteins (Huang et al, 2014). The effect of nicotine on S. epidermidis and gene regulation remains unclear
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