4.7 Article

The specific anti-biofilm effect of gallic acid on Staphylococcus aureus by regulating the expression of the ica operon

Journal

FOOD CONTROL
Volume 73, Issue -, Pages 613-618

Publisher

ELSEVIER SCI LTD
DOI: 10.1016/j.foodcont.2016.09.015

Keywords

Gallic acid; Staphylococcus aureus; Anti-biofilm; ica operon; Food industry

Funding

  1. National Natural Science Foundation of China [31301472]
  2. Fundamental Research Funds for the Central University [GIC201601002]
  3. Shaanxi province science and technology co-ordinating innovative engineering projects [2015KTZDNY01-07]

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Staphylococcus aureus (S. aureus) biofilms are of considerable interest in food safety because biofilms can increase the risk of food contamination and enhance the pathogenicity of bacteria. The ica-encoded polysaccharide intercellular adhesin (PIA) plays an important role in biofilm formation. In this study, the MIC of gallic acid against S. aureus in suspension and in biofilms was 2 mg/mL and 4 mg/mL, respectively. Quantitative crystal violet staining of biofilms showed that 2 mg/mL gallic acid can effectively inhibit biofilm formation and the ESEM images clearly showed the three-dimensional biofilm morphology of the S. aureus and the resulting anti-biofilm effect. The determination of viable bacteria in the biofilm revealed that gallic acid penetrated the biofilm to kill S. aureus, the bactericidal effect on the biofilm bacteria was comparable to that of planktonic bacteria. We further explored the influence of gallic acid on ica family gene expression and polysaccharide slime formation in S. aureus biofilm formation. The results showed that icaR was significantly activated that; icaA and icaD were downregulated in a dose dependent manner with increasing concentrations of gallic acid; however, the expression of icaB and icaC was not significantly affected. The polysaccharide slime formation was reduced as well. Based on these results, gallic acid, as a natural substance, may play an important role in the food industry. (C) 2016 Elsevier Ltd. All rights reserved.

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