Hyperoside inhibits biofilm formation of Pseudomonas aeruginosa

Abstract

Abstract. Pseudomonas aeruginosa (P. aeruginosa) is a common pathogen in hospital-acquired infection and is readily able to form biofilms. Due to its high antibiotic resistance, traditional antibacterial treatments exert a limited effect on P. aeruginosa biofilm infections. It has been indicated that hyperoside inhibits P. aeruginosa PAO1 (PAO1) biofilm formation without affecting growth. Therefore, the current study examined the biofilm formation and quorum sensing (QS) system of PAO1 in the presence of hyperoside.Confocal laser scanning microscopy analysis demonstrated that hyperoside significantly inhibited biofilm formation. It was also observed that hyperoside inhibited twitching motility in addition to adhesion. Data from reverse transcription-quantitative polymerase chain reaction indicated that hyperoside inhibited the expression of lasR, lasI, rhlR and rhlI genes. These results suggest that the QS-inhibiting effect of hyperoside may lead to a reduction in biofilm formation. However, the precise mechanism of hyperoside on P. aeruginosa pathogenicity remains unclear and requires elucidation in additional studies. IntroductionPseudomonas aeruginosa (P. aeruginosa) is a common pathogen in hospital-acquired infections (1). Due to increasing multidrug resistance, P. aeruginosa infection is an increasingly common cause of mortality and morbidity (2). The mechanisms of antibiotic resistance in P. aeruginosa include the expression of multiple antibiotic modifying enzymes, antibiotic efflux pumps and acquisition of chromosomally or plasmid encoded antibiotic resistance genes. Additionally, chromosomal mutations and lower membrane permeability for the antibiotics also contribute to antibiotic resistance (3).P. aeruginosa is a biofilm-forming pathogen and is difficult to eradicate due to its high antibiotic resistance and the ability of the biofilm to evade the immune system (4-7). Quorum sensing (QS) is a system of stimuli and response correlated to population density. P. aeruginosa uses the QS system to coordinate gene expression according to the density of its local population. Thus, it can coordinate certain behaviors such as biofilm formation, virulence and antibiotic resistance. QS inhibitors (QSIs) are the most well reported alternative therapeutics that can be used to overcome the problem of increasing antibiotic resistance in P. aeruginosa. QSIs target the virulence of the organism and therefore are also termed antipathogenic drugs. The virulence of P. aeruginosa depends on its cell-to-cell communication system, or QS system that uses diffusible signaling molecules that accumulate with increasing cell density and allows P. aeruginosa to trigger coordinated responses and achieve outcomes that would otherwise remain impossible to achieve by individual bacterium (8). Previous studies have demonstrated that traditional treatments for bacteria exert some effect on biofilm infections (9,10). Therefore, the effects of constituents from marine organisms, traditional Chinese herbs and plants (11-13) on biofilm infe...

Hyperoside protects against cerebral ischemia-reperfusion injury by alleviating oxidative stress, inflammation and apoptosis in rats

“…Hyperoside, also known as quercetin-3-O-b-D-galactopyranoside, is found in the fruit or whole plant of Hypericaceae, Rosaceae, Campanulaceae and Celastraceae plants, and belongs to the group of flavonol glycosides, with hepatoprotective, anticancer, bacteriostatic and memory-improving properties [7][8][9]. In addition, hyperoside can protect against myocardial I/R injury by inhibiting endoplasmic reticulum stress and activating the Nrf2 signalling pathway [10].…”

Quorum quenchers affect the virulence regulation of non-mucoid, mucoid and heavily mucoid biofilms co-cultured on cell lines

“…Both adhesion and formation of biofilms depend primarily on motility (Sun et al, 2017 ). Swimming, swarming and twitching are three forms of motility in P. aeruginosa that are positively controlled by the LasIR and RhIR QS systems; las regulating swimming, swarming and twitching; and rhI controlling swarming and twitching (Yeung et al, 2009 ).…”

<p>Effect of Sub-Minimum Inhibitory Concentrations of Tyrosol and EDTA on Quorum Sensing and Virulence of <em>Pseudomonas aeruginosa</em></p>

“…Motility is an important factor in both adhesion and biofilm formation. 65 P. aeruginosa has three types of motility that are swimming, swarming and twitching which are positively regulated by both LasIR and RhIR QS systems, where las control swimming, swarming and twitching and rhI regulates swarming and twitching. 66 In this study both swimming and swarming motility were significantly attenuated by tyrosol (1/4x - 1/16x MIC) and EDTA (1/4x and 1/8x MIC).…”