In the PQS-MvfR system, 2-heptyl-3-hydroxy-4(1H) quinolone (PQS) and its precursors bind to the transcriptional regulator MvfR and control the transcription of downstream targets 13. LasR and RhlR transcriptional regulators are activated when sufficient levels of OdDHL and BHL are present resulting from a high population density of P. 1a) which can bind to its cognate transcriptional regulator RhlR. Likewise, RhlI produces the N-butyryl-L-homoserine lactone (BHL) signal molecule ( Fig. OdDHL is recognized by the transcriptional regulator LasR which directs various gene expressions including genes affecting the RhlI-RhlR system. LasI produces an extracellular diffusible AHL signal molecule, N-(3-oxododecanoyl)-L-homoserine lactone (OdDHL) shown in Fig. aeruginosa has three main QS systems: LasI-LasR, RhlI-RhlR and PQS-MvfR. aeruginosa use N-acylated homoserine lactones (AHLs) as AI molecules. Chemical signal molecules called autoinducers (AIs) increase in concentration with population density and are received by transcriptional regulators that control gene expression 10. QS is a signal and response based system dependent on population density. Quorum sensing (QS) is a bacterial communication system for coordinating group behaviors such as forming biofilms and producing virulence factors.
A means to control biofilm growth to more effectively treat P. aeruginosa are reported to be more resistant to antibiotics and biocides than planktonic cells, which often cause difficulties in eradicating them from patients infected with the bacterium 9. aeruginosa can colonize on various surfaces by forming a biofilm in which bacterial cells stick together and are embedded within a self-produced extracellular polysaccharide matrix 8.
#Gingerol chem draw skin
aeruginosa is observed in diverse natural and man-made environments such as natural water bodies, soil, skin and many medical devices 6, 7. In particular, it is fatal to cystic fibrosis patients, the most common genetic disorder in Caucasians 4, by forming mucoid in lung tissue leading to pneumonia 5. It infects pulmonary and urinary tracts, burns and wounds, sometimes resulting in serious health complications 2, 3. P seudomonas aeruginosa is a notorious opportunistic and nosocomial pathogenic bacterium infecting immunocompromised patients 1.
These results strongly support our hypothesis and offer insight into the molecular mechanism that caused QS gene repression.
Further transcriptome analyses demonstrated that 6-gingerol successfully repressed QS-induced genes, specifically those related to the production of virulence factors.
Experimentally 6-gingerol reduced biofilm formation, several virulence factors (e.g., exoprotease, rhamnolipid and pyocyanin) and mice mortality. In silico studies demonstrated molecular binding occurs between 6-gingerol and the QS receptor LasR through hydrogen bonding and hydrophobic interactions. Here we tested the hypothesis that 6-gingerol, a pungent oil of fresh ginger, reduces biofilm formation and virulence by antagonistically binding to P. Interfering with normal QS interactions between signal molecules and their cognate receptors is a developing strategy for attenuating its virulence. Pseudomonas aeruginosa is a well-known pathogenic bacterium that forms biofilms and produces virulence factors via quorum sensing (QS).
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