Anti-biofilm Activities from Resveratrol against Fusobacterium nucleatum.

Zhiyan He,Zisheng Tang,Wei Zhou,Zhengwei Huang,Jingping Liang,Rui Ma

doi:10.3389/fmicb.2016.01065

Abstract

Fusobacterium nucleatum is a Gram-negative, anaerobic bacterium that plays an important role in dental plaque biofilm formation. In this study, we evaluate the effect of resveratrol, a phytoalexin compound, on F. nucleatum biofilm formation. The effects of different concentrations of resveratrol on biofilms formed on 96-well microtiter plates at different time points were determined by the MTT assay. The structures and thicknesses of the biofilm were observed by confocal laser scanning microscopy (CLSM), and gene expression was investigated by real-time PCR. The results showed that resveratrol at sub-MIC levels can significantly decrease biofilm formation, whereas it does not affect the bacterial growth rate. It was observed by CLSM images that the biofilm was visually decreased with increasing concentrations of resveratrol. Gene expression was down regulated in the biofilm in the presence of resveratrol. Our results revealed that resveratrol can effectively inhibit biofilm formation.

Highlights

In natural and industrial environments, bacteria mostly grow as biofilms attached to surfaces or are associated with interfaces, where bacterial cells are encased in a self-produced extracellular polymeric matrix
The effect of resveratrol on biofilm formation was evaluated when F. nucleatum was grown in 96-well plates of polystyrene
With increasing concentrations of resveratrol, the biofilms formed by F. nucleatum exhibited OD590 nm values that decreased from 0.347 ± 0.038 at 1.5625 μg ml−1 to 0.136 ± 0.018 at 25 μg ml−1 after a 24 h incubation

Summary

Introduction

In natural and industrial environments, bacteria mostly grow as biofilms attached to surfaces or are associated with interfaces, where bacterial cells are encased in a self-produced extracellular polymeric matrix. The first step involves the adherence of the bacterial cells to the host surface; subsequently, adherent cells form a multilayer biofilm covered by an extracellular matrix (Flemming and Wingender, 2010; Trappetti et al, 2011; Srinandan et al, 2015). After incorporation into the biofilm, microorganisms are resistant to host defense mechanisms, such as phagocytosis, and to antimicrobial agents. This change has been suggested to be involved in the persistence of infection by such microorganisms (Costerton et al, 1999; Jacqueline and Caillon, 2014)

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Conclusion