Nicotine Enhances Staphylococcus epidermidis Biofilm Formation by Altering the Bacterial Autolysis, Extracellular DNA Releasing, and Polysaccharide Intercellular Adhesin Production

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 ba...

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Veröffentlicht in:Frontiers in microbiology 2018-10, Vol.9, p.2575-2575
Hauptverfasser: Wu, Yang, Ma, Yue, Xu, Tao, Zhang, Qing-Zhao, Bai, Jinna, Wang, Jiaxue, Zhu, Tao, Lou, Qiang, Götz, Friedrich, Qu, Di, Zheng, Chun-Quan, Zhao, Ke-Qing
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Sprache:eng
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Zusammenfassung: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 biofilm is still unclear. In this study, we tested the effect of nicotine, one of the most active components of tobacco, on biofilm formation, and we studied the underlying mechanisms. Our results showed that nicotine promoted the biofilm formation of 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 , and , nicotine induced increase in biofilm formation was similar to that in SE1457; but in , and , the effect was obviously impaired. Consistently, the increase of the bacterial autolysis rate in and 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 and restored by the complementation. The 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 biofilm formation by promoting its initial attachment and intercellular accumulation; the , and genes mediating bacterial autolysis and PIA production play an important role in this process.
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2018.02575