Antimicrobial mechanism and the effect of atmospheric pressure N2 plasma jet on the regeneration capacity of Staphylococcus aureus biofilm. Issue 8 (14th September 2018)

• Record Type: Journal Article
• Authors: Wang, Jiaquan; Yu, Zhiyuan; Xu, Zimu; Hu, Shuheng; Li, Yunxia; Xue, Xiaojuan; Cai, Qiuchen; Zhou, Xiaoxia; Shen, Jie; Lan, Yan; Cheng, Cheng
• Is Part Of: Biofouling. Volume 34:Issue 8(2018)
• Page Start: 935
• Page End: 949
• Publication Date: 2018-09-14
• Subjects: Atmospheric-pressure plasma jet (APPJ) -- Staphylococcus aureus biofilm -- reactive oxygen species (ROS) -- biofilm regeneration capacity; Marine fouling organisms -- Periodicals; Materials -- Biodeterioration -- Periodicals; Fouling -- Periodicals; Biodegradation -- Periodicals; Environmental Microbiology -- Periodicals; Water Microbiology -- Periodicals; 576.165
• DOI: 10.1080/08927014.2018.1530350
• Languages: English
• ISSNs: 0892-7014

Abstract

Abstract: This study systematically assessed the inactivation mechanism on Staphylococcus aureus biofilms by a N2 atmospheric-pressure plasma jet and the effect on the biofilm regeneration capacity from the bacteria which survived, and their progenies. The total bacterial populations were 7.18 ± 0.34 log10 CFU ml −1 in biofilms and these were effectively inactivated (>5.5-log10 CFU ml −1 ) within 30 min of exposure. Meanwhile, >80% of the S. aureus biofilm cells lost their metabolic capacity. In comparison, ∼20% of the plasma-treated bacteria entered a viable but non-culturable state. Moreover, the percentage of membrane-intact bacteria declined to ∼30%. Scanning electron microscope images demonstrated cell shrinkage and deformation post-treatment. The total amount of intracellular reactive oxygen species was observed to have significantly increased in membrane-intact bacterial cells with increasing plasma dose. Notably, the N2 plasma treatment could effectively inhibit the biofilm regeneration ability of the bacteria which survived, leading to a long-term phenotypic response and dose-dependent inactivation effect on S. aureus biofilms, in addition to the direct rapid bactericidal effect.