Suppression of Virulence Factors in Pseudomonas Aeruginosa Clinical Isolates through Natural Compound-Mediated Quorum Sensing Inhibition
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Abstract
Opgective: The pathogenesis of Pseudomonas aeruginosa dependent on a number of virulence factors that help to enable for host colonization. Among the virulence factors: biofilm, pyocyanin, elastase and protease. The problem of antibiotic resistance in P. aeruginosa is highly significant due to its possession of mechanisms and enzymes that assist in resistance. Consequently, reducing resistance and the pathogenicity of these bacteria is the objective of many researchers. This study aims to utilize natural compounds and examine their effects in inhibiting certain virulence factors of P. aeruginosa (elastase and protease) by decreasing the gene expression of the regulatory system that controls the production of virulence factors and bacterial pathogenicity, without impacting bacterial growth.
Methods: samples were diagnosed and verified using the Vitek-2 system. minimum inhibitory concentration (MIC) of cinnamonaldehyde (CA) and salicylic acid (SA) against P. aeruginosa isolates was determined. The sub-MIC concentrations of CA and SA were utilized to quantify their inhibitory effect on proteases and elastase in the presence and absence of these compounds, as well as the expression levels of the LasI and RhlR genes. Quantitative real-time PCR was utilized to detect a reduction in LasI and RhlR expression.
Result: Protease mean decreased with SA to 0.05 (±0.059) and with CA to 0.08 (±0.050) from 0.43 (±0.22) to 0.05 (±0.059). Additionally, the mean elastase was decreased with SA to 0.1138 (± 0.151) and with CA to 0.2 (± 0.217). Whereas SA and CA changed the expression level of LasI from 1 to 0.3 and 1.3 folds, respectively, the expression level of RhlR was reduced from 1 to 0.5 and 0.2 folds.
Conclusion: Natural compounds CA and SA significantly reduced the phenotypic virulence factors; protease, elastase and reducing the expression of the RhlR and lasl genes in p. aeruginosa.