article · Antibiotics
Pseudomonas aeruginosa frequently develops resistance to standard antimicrobial therapies, often through specialised efflux pumps that expel medications from bacterial cells. This laboratory study evaluated cinnamon essential oil, tested against extensive drug-resistant and pan drug-resistant isolates collected from human and animal sources. Over 70 percent of tested samples carried P. aeruginosa, with nearly half identified as multidrug-resistant. Cinnamon essential oil demonstrated clear antibacterial effects across all tested resistant isolates, producing notable inhibition zones and low minimum inhibitory and bactericidal concentrations. In addition to direct antibacterial action, phenotypic tests indicated a two-fold reduction in efflux pump activity following exposure to the oil. Genetic analysis confirmed this mechanism, showing statistically significant reductions in the expression levels of the resistance-associated genes MexA and MexB, highlighting the oil as an active agent against bacterial resistance mechanisms.
Drug-resistant Pseudomonas aeruginosa infections in humans and animals are difficult to treat because the bacteria pump conventional antibiotics out of their cells. Identifying natural compounds that simultaneously kill resistant bacteria and suppress their cellular defence mechanisms provides new leads for developing treatments to combat growing antimicrobial resistance.
This work points to prospective therapeutic applications for pharmaceutical developers seeking plant-derived antibacterial agents and efflux pump inhibitors. Potential users include antimicrobial drug discovery teams tackling resistant human and animal infections. Given that findings are currently restricted to in vitro phenotypic and gene expression assays, the research is at an early laboratory stage and requires further translational testing before commercial formulation.
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Pseudomonas aeruginosa is notorious for its ability to develop a high level of resistance to antimicrobial agents. Resistance-nodulation-division (RND) efflux pumps could mediate drug resistance in P. aeruginosa. The present study aimed to evaluate the antibacterial and anti-efflux activities of cinnamon essential oil either alone or combined with ciprofloxacin against drug resistant P. aeruginosa originated from human and animal sources. The results revealed that 73.91% of the examined samples were positive for P. aeruginosa; among them, 77.78% were of human source and 72.73% were recovered from animal samples. According to the antimicrobial resistance profile, 48.73% of the isolates were multidrug-resistant (MDR), 9.2% were extensive drug-resistant (XDR), and 0.84% were pan drug-resistant (PDR). The antimicrobial potential of cinnamon oil against eleven XDR and one PDR P. aeruginosa isolates was assessed by the agar well diffusion assay and broth microdilution technique. The results showed strong antibacterial activity of cinnamon oil against all tested P. aeruginosa isolates with inhibition zones’ diameters ranging from 34 to 50 mm. Moreover, the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values of cinnamon oil against P. aeruginosa isolates ranged from 0.0562–0.225 µg/mL and 0.1125–0.225 µg/mL, respectively. The cinnamon oil was further used to evaluate its anti-efflux activity against drug-resistant P. aeruginosa by phenotypic and genotypic assays. The cartwheel test revealed diminished efflux pump activity post cinnamon oil exposure by two-fold indicating its reasonable impact. Moreover, the real-time quantitative polymerase chain reaction (RT-qPCR) results demonstrated a significant (p < 0.05) decrease in the expression levels of MexA and MexB genes of P. aeruginosa isolates treated with cinnamon oil when compared to the non-treated ones (fold changes values ranged from 0.4204–0.7474 for MexA and 0.2793–0.4118 for MexB). In conclusion, we suggested the therapeutic use of cinnamon oil as a promising antibacterial and anti-efflux agent against drug-resistant P. aeruginosa.
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DOI: 10.3390/antibiotics12101514
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