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Author Spotlight: Advancing Therapeutics to Treat Vibriosis in Humans and Aquatic Organisms
Published on: May 31, 2024
Investigation of Pseudomonas aeruginosa quorum-sensing signaling system for identifying multiple inhibitors using
Vahid Soheili1, Bibi Sedigheh Fazly Bazzaz2, Nooshin Abdollahpour3
1Department of Drug and Food Control, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
Abstract:
Pseudomonas aeruginosa is an opportunistic human pathogen and a common Gram-negative bacterium in hospital-acquired infections. It causes death in many burn victims, cystic-fibrosis and neutropenic-cancer patients. It is known that P. aeruginosa biofilm maturation and production of cell-associated and extracellular virulence factors such as pyocyanin, elastase and rhamnolipids are under the control of a quorum-sensing (QS) system. Among several proteins involved in the Pseudomonas QS mechanism, LasR and PqsE play an important role in its cascade signaling system. They can cause increases in QS factors, biofilm maturation, and the production of virulence factors. Therefore, inhibition of these proteins can reduce the pathogenicity of P. aeruginosa. According to the structure of corresponding auto-inducers bound to these proteins, in silico calculations were performed with some non-steroidal anti-inflammatory drugs (NSAIDs) to estimate possible interactions and find the co-inhibitors of LasR and PqsE. The results showed that oxicams (Piroxicam and Meloxicam) can interact well with active sites of both proteins with the Ki of 119.43 nM and 4.0 μM for Meloxicam and 201.39 nM and 4.88 μM against LasR and PqsE, respectively. These findings suggested that Piroxicam and Meloxicam can be used as potential inhibitors for control of the P. aeruginosa QS signaling system and biofilm formation, and may be used in the design of multiple inhibitors.
Insights
Non-steroidal anti-inflammatory drugs, specifically Piroxicam and Meloxicam, show potential for inhibiting Pseudomonas aeruginosa quorum-sensing. These drugs may offer a new strategy to combat infections and biofilm formation caused by this opportunistic pathogen.
Area of Science:
- Microbiology
- Pharmacology
- Computational Biology
Background:
- Pseudomonas aeruginosa is a significant opportunistic pathogen causing severe hospital-acquired infections, particularly in vulnerable patients.
- Bacterial virulence and biofilm formation in P. aeruginosa are regulated by a quorum-sensing (QS) system, involving key proteins like LasR and PqsE.
- Inhibiting LasR and PqsE is a promising strategy to reduce P. aeruginosa pathogenicity.
Purpose of the Study:
- To investigate the potential of non-steroidal anti-inflammatory drugs (NSAIDs) as co-inhibitors for the Pseudomonas aeruginosa QS proteins, LasR and PqsE.
- To evaluate the in silico interaction of NSAIDs with the active sites of LasR and PqsE.
Main Methods:
- In silico computational analysis was employed to assess the binding interactions of selected NSAIDs with the auto-inducer binding sites of LasR and PqsE.
- The binding affinity (Ki values) of potential inhibitors against both target proteins was calculated.
Main Results:
- Oxicam-class NSAIDs, specifically Piroxicam and Meloxicam, demonstrated favorable interactions with the active sites of both LasR and PqsE.
- Meloxicam exhibited Ki values of 119.43 nM for LasR and 4.0 μM for PqsE.
- Piroxicam showed Ki values of 201.39 nM for LasR and 4.88 μM for PqsE.
Conclusions:
- Piroxicam and Meloxicam are identified as potential inhibitors of the P. aeruginosa QS signaling pathway.
- These NSAIDs may serve as lead compounds for developing novel therapeutic agents to control P. aeruginosa infections and biofilm formation.
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