Extraction optimization and bioactivities of an extracellular polysaccharide produced by Aspergillus fumigatus

et al. 2019

J Appl Microbiol

Aim The objective of this study was to investigate the biofilm inhibitory activity of Streptomyces‐derived actinomycin D against biofilm formation by Staphylococcus epidermidis. Methods and Results The microtitre plate method and microscopy were used to detect the biofilm formation of S. epidermidis. And an attempt was made to detect the effect of actinomycin D on important biofilm components, exopolysaccharides (EPS) in S. epidermidis using precolumn derivation HPLC. Also cell surface hydrophobicities of S. epidermidis were assessed to explore action mechanisms. The qPCR was performed to demonstrate the genetic mechanisms of biofilm formation by S. epidermidis. Unlike other antibiotics, actinomycin D (1·5 μg ml−1) from Streptomyces luteus significantly inhibited biofilm formation by S. epidermidis. Additionally, it effectively inhibited S. epidermidis cells from adhering to glass slides. Actinomycin D downregulated ica locus and then the reduced polysaccharide intercellular adhesin production caused S. epidermidis cells to become less hydrophobic, thus supporting its anti‐biofilm effect. Conclusion Streptomyces‐derived actinomycin D is active in inhibiting the biofilm formation of S. epidermidis. Significance and Impact of the Study Actinomycin D can be used as a promising antibiofilm agent in inhibiting S. epidermidis biofilm formation. The study is also the first insight into how actinomycin D inhibited the biofilm formation of S. epidermidis. Actinomycin D could potentially be used to reduce the risk of biofilm‐associated infections. Our study also suggests that the metabolites from Actinomycete strains keep further attention as potential antibiofilm agents against biofilm formation of S. epidermidis, even biofilm infections of the other bacteria.

Section: Methodsmentioning

confidence: 99%

Streptomyces ‐derived actinomycin D inhibits biofilm formation via downregulating ica locus and decreasing production of PIA in Staphylococcus epidermidis

Xie

et al. 2019

J Appl Microbiol

“…EPS in the S. epidermidis culture was collected by water extraction and alcohol precipitation (Jin and Zhao ). To remove proteins, proteinase K and n ‐butyl alcohol (5 : 1, 71‐36‐3; BOC Sciences, New York, NY, USA) were used as described previously (Li et al .…”

Section: Methodsmentioning

confidence: 99%

Antibiofilm activity of threeActinomycetestrains againstStaphylococcus epidermidis

Xie

Ren

et al. 2018

Lett Appl Microbiol

Significance and Impact of the Study: Staphylococcus epidermidis infections are frequently associated with biofilms that are difficult to eradicate with conventional antibiotics. The new biofilm inhibitors from Actinomycete will have a great value in the prevention and treatment of dairy cow mastitis and other biofilm-related infections. AbstractThis study sought to identify novel and nontoxic biofilm inhibitors from the Actinomycete library for attenuating biofilm formation by Staphylococcus epidermidis. After investigating the antibiofilm activities of spent media from 185 Actinomycete strains using two S. epidermidis strains (ATCC 35984 and a clinical strain 5-121-2) as target bacteria, three strains of tested Actinomycete (TRM 46200, TRM 41337, and TRM 46814) showed a significant inhibition against S. epidermidis biofilm formation without affecting the growth of planktonic cells. The characteristics of three strains of supernatants suggested that hydrophilic compound possibly extracellular peptides or proteins from these three strains, confer the biofilm reduction in S. epidermidis. An attempt was made to assess their effects on biofilm components and cell surface hydrophobicities in order to disclose acting mechanisms. The crude proteins from spent media of three strains degraded not only exopolysaccharides but also extracellular DNA in S. epidermidis biofilm. The active substances in crude proteins caused S. epidermidis cells to become less hydrophobic. Given these results, the metabolites from Actinomycete strains should keep further attention as potential antibiofilm agents against biofilm formation of S. epidermidis, even biofilm infections of the other bacteria.

“…To quantify the exopolysaccharides (EPS) produced by S. epidermidis, the cells were diluted 1:100 with fresh TSB and cultured for 24 h with shaking at 37 • C. Then, the water extraction and alcohol precipitation method was used to collect EPS as previously described, with slight modifications (Petit and Pinilla, 1995;Li et al, 2011;Jin and Zhao, 2014), and air-dried at room temperature. The crude polysaccharides were dissolved by 0.5 mol L −1 hydrochloric acid and 121 • C heat treated for 15 min.…”

Section: Effect Of Quercetin On the Production And Components Of Exopmentioning

confidence: 99%

Quercetin Inhibits Biofilm Formation by Decreasing the Production of EPS and Altering the Composition of EPS in Staphylococcus epidermidis

Chen

2021

Front. Microbiol.

Staphylococcus epidermidis is an opportunistic pathogen, and its biofilm formation ability is an important virulent factor. Quercetin, a typical flavonoid ubiquitously used in dietary supplementation, is known for its antioxidant property, but its anti-biofilm activity against S. epidermidis remains unknown. In this study, the anti-biofilm activity of quercetin was investigated using S. epidermidis ATCC35984, a strong biofilm-positive strain. An attempt was made to disclose the mechanisms of the anti-biofilm activity of quercetin. S. epidermidis exhibited a less cell surface hydrophobicity after quercetin treatment. Also, quercetin effectively inhibited S. epidermidis cells from adhering to the glass slides. Quercetin downregulated the intercellular adhesion (ica) locus and then polysaccharide intercellular adhesin (PIA) production was reduced. Therefore, S. epidermidis cells became less hydrophobic, which supported quercetin’s anti-biofilm effect. Our study suggests that quercetin from plants be given further attention as a potential anti-biofilm agent against the biofilm formation of S. epidermidis, even biofilm infections of other bacteria.