Resveratrol Oligomers Inhibit Biofilm Formation of <i>Escherichia coli</i> O157:H7 and <i>Pseudomonas aeruginosa</i>

Biofilm formation is closely related to bacterial infection and is also a mechanism of antimicrobial resistance. Hence, the antibiofilm approach provides an alternative to an antibiotic strategy. In this study, the antibiofilm activities of resveratrol (<b>1</b>) and five of its oligomers, namely, ε-viniferin (<b>2</b>), suffruticosol A (<b>3</b>), suffruticosol B (<b>4</b>), vitisin A (<b>5</b>), and vitisin B (<b>6</b>), were investigated against enterohemorrhagic <i>Escherichia coli</i> O157:H7 and <i>Pseudomonas aeruginosa</i> PA14. Vitisin B (<b>6</b>), a stilbenoid tetramer, was found to inhibit biofilm formation by the two bacteria the most effectively and at 5 μg/mL inhibited <i>E. coli</i> O157:H7 biofilm formation by more than 90%

Inhibitory effects of the essential oils α-longipinene and linalool on biofilm formation and hyphal growth of <i>Candida albicans</i>

<p><i>Candida albicans</i> is one of the most common fungal pathogens, and causes systemic and invasive infections in humans. <i>C. albicans</i> biofilms are composed of yeast and hyphal and pseudohyphal elements, and the transition of yeast to the hyphal stage could be a virulence factor. In this study, diverse essential oils were initially investigated for anti-biofilm activity against <i>C. albicans</i> strains, and cascarilla bark oil and helichrysum oil and their components α-longipinene (a major constituent of both) and linalool were found to markedly inhibit biofilm formation without affecting planktonic cell growth. Moreover, α-longipinene and linalool were found to synergistically reduce biofilm formation. Notably, treatments with cascarilla bark oil, helichrysum oil, α-longipinene, or linalool clearly inhibited hyphal formation, and this appeared to be largely responsible for their anti-biofilm effect. Furthermore, the two essential oils, α-longipinene and linalool, reduced <i>C. albicans</i> virulence in <i>Caenorhabditis elegans</i>.</p

‘Should I stay or should I go?’ Bacterial attachment <i>vs</i> biofilm formation on surface-modified membranes

<div><p>A number of techniques are used for testing the anti-biofouling activity of surfaces, yet the correlation between different results is often questionable. In this report, the correlation between initial bacterial deposition (fast tests, reported previously) and biofilm growth (much slower tests) was analyzed on a pristine and a surface-modified reverse osmosis membrane ESPA-1. The membrane was modified with grafted hydrophilic polymers bearing negatively charged, positively charged and zwitter-ionic moieties. Using three different bacterial strains it was found that there was no general correlation between the initial bacterial deposition rates and biofilm growth on surfaces, the reasons being different for each modified surface. For the negatively charged surface the slowest deposition due to the charge repulsion was eventually succeeded by the largest biofilm growth, probably due to secretion of extracellular polymeric substances (EPS) that mediated a strong attachment. For the positively charged surface, short-term charge attraction by quaternary amine groups led to the fastest deposition, but could be eventually overridden by their antimicrobial activity, resulting in non-consistent results where in some cases a lower biofilm formation rate was observed. The results indicate that initial deposition rates have to be used and interpreted with great care, when used for assessing the anti-biofouling activity of surfaces. However, for a weakly interacting ‘low-fouling’ zwitter-ionic surface, the positive correlation between initial cell deposition and biofilm growth, especially under flow, suggests that for this type of coating initial deposition tests may be fairly indicative of anti-biofouling potential.</p></div

Table_1_Herring Oil and Omega Fatty Acids Inhibit Staphylococcus aureus Biofilm Formation and Virulence.docx

<p>Staphylococcus aureus is notorious for its ability to become resistant to antibiotics and biofilms play a critical role in antibiotic tolerance. S. aureus is also capable of secreting several exotoxins associated with the pathogenesis of sepsis and pneumonia. Thus, the objectives of the study were to examine S. aureus biofilm formation in vitro, and the effects of herring oil and its main components, omega fatty acids [cis-4,7,10,13,16,19-docosahexaenoic acid (DHA) and cis-5,8,11,14,17-eicosapentaenoic acid (EPA)], on virulence factor production and transcriptional changes in S. aureus. Herring oil decreased biofilm formation by two S. aureus strains. GC-MS analysis revealed the presence of several polyunsaturated fatty acids in herring oil, and of these, two omega-3 fatty acids, DHA and EPA, significantly inhibited S. aureus biofilm formation. In addition, herring oil, DHA, and EPA at 20 μg/ml significantly decreased the hemolytic effect of S. aureus on human red blood cells, and when pre-treated to S. aureus, the bacterium was more easily killed by human whole blood. Transcriptional analysis showed that herring oil, DHA, and EPA repressed the expression of the α-hemolysin hla gene. Furthermore, in a Caenorhabditis elegans nematode model, all three prolonged nematode survival in the presence of S. aureus. These findings suggest that herring oil, DHA, and EPA are potentially useful for controlling persistent S. aureus infection.</p

<i>Streptomyces</i>-derived actinomycin D inhibits biofilm formation by <i>Staphylococcus aureus</i> and its hemolytic activity

<p><i>Staphylococcus aureus</i> is a versatile human pathogen that produces diverse virulence factors, and its biofilm cells are difficult to eradicate due to their inherent ability to tolerate antibiotics. The anti-biofilm activities of the spent media of 252 diverse endophytic microorganisms were investigated using three <i>S. aureus</i> strains. An attempt was made to identify anti-biofilm compounds in active spent media and to assess their anti-hemolytic activities and hydrophobicities in order to investigate action mechanisms. Unlike other antibiotics, actinomycin D (0.5 μg ml⁻¹) from <i>Streptomyces parvulus</i> significantly inhibited biofilm formation by all three <i>S. aureus</i> strains. Actinomycin D inhibited slime production in <i>S. aureus</i> and it inhibited hemolysis by <i>S. aureus</i> and caused <i>S. aureus</i> cells to become less hydrophobic, thus supporting its anti-biofilm effect. In addition, surface coatings containing actinomycin D prevented <i>S. aureus</i> biofilm formation on glass surfaces. Given these results, FDA-approved actinomycin D warrants further attention as a potential antivirulence agent against <i>S. aureus</i> infections.</p