Abstract
Pseudomonas aeruginosa is an opportunistic pathogen that causes high morbidity and mortality rates due to its biofilm form. Biofilm formation is regulated via quorum sensing (QS) mechanism and provides up to 1000 times more resistance against conventional antibiotics. QS related genes are expressed according to bacterial population density via signal molecules. QS inhibitors (QSIs) from natural sources are widely studied evaluating various extracts from extreme environments. It is suggested that extremely halophilic Archaea may also produce QSI compounds. For this purpose, we tested QS inhibitory potentials of ethyl acetate extracts from cell free supernatants and cells of Natrinema versiforme against QS and biofilm formation of P. aeruginosa. To observe QS inhibition, all extracts were tested on P. aeruginosa lasB-gfp, rhlA-gfp, and pqsA-gfp biosensor strains and biofilm inhibition was studied using P. aeruginosa PAO1. According to our results, QS inhibition ratios of cell free supernatant extract (CFSE) were higher than cell extract (CE) on las system, whereas CE was more effective on rhl system. In addition, anti-biofilm effect of CFSE was higher than CE. Structural analysis revealed that the most abundant compound in the extracts was trans 4-(2-carboxy-vinyl) benzoic acid.
Highlights
Multidrug-resistant and extensively drug-resistant microorganisms arise from increased and uncontrolled antibiotic utilization (Gohil et al, 2018)
The compounds which have been reported to have quorum sensing (QS) inhibitory potentials are cyclo (LPro-L-Phe) and cyclo (L-Pro-L-isoLeu) from Marinobacter sp. (SK-3); phenethylamides and a cyclic dipeptide isolated from Halobacillus salinus, Bacillus or Halobacillus sp.; palmitic acid from Synechococcus elongatus (Abed et al, 2013; Santhakumari et al, 2016, 2017)
Our knowledge about QS system and potential quorum quenching (QQ) in extremophiles guided us to hypothesize that extremophilic microorganisms can adapt to harsh conditions by producing some other unstudied metabolites to compete with other organisms
Summary
Multidrug-resistant and extensively drug-resistant microorganisms arise from increased and uncontrolled antibiotic utilization (Gohil et al, 2018). Treatment of infections caused by Pseudomonas aeruginosa can be complicated due to its acquired multidrug resistance, its virulence factors and biofilm formation resulting in communityacquired and hospital-acquired infections (Singh et al, 2000; Smith and Iglewski, 2003; Bjarnsholt et al, 2010). This opportunistic pathogen causes nearly 11% of nosocomial infections especially in immunocompromised patients with cystic fibrosis (CF), pneumonia, urinary tract infections, surgical site infections, sepsis, and skin infections especially observed in burn units. Thereby, pathogenic bacteria can fight against the host immune system by the collective expression of virulence genes (Papenfort and Bassler, 2016)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
