AI Article Synopsis

  • The pathogen discussed causes various infections, especially in people with weakened immune systems, and exhibits drug resistance through quorum sensing (QS) mechanisms, which affect its pathogenicity.* -
  • Selenium nanoparticles (SeNPs) show potential as a treatment for these infections, despite limited existing research on their mechanisms and interactions with QS signaling proteins.* -
  • The study uses computational methods to demonstrate that SeNPs effectively bind to key QS proteins, potentially inhibiting their function and blocking the production of harmful signaling molecules, thereby reducing the pathogen's virulence.*

Article Abstract

is an infectious pathogen which has the ability to cause primary and secondary contagions in the blood, lungs, and other body parts of immunosuppressed individuals, as well as community-acquired diseases, such as folliculitis, osteomyelitis, pneumonia, and others. This opportunistic bacterium displays drug resistance and regulates its pathogenicity via the quorum sensing (QS) mechanism, which includes the LasI/R, RhlI/R, and PQS/MvfR systems. Targeting the QS systems might be an excellent way to treat infections. Although a wide array of antibiotics, namely, newer penicillins, cephalosporins, and combination drugs are being used, the use of selenium nanoparticles (SeNPs) to cure infections is extremely rare as their mechanistic interactions are weakly understood, which results in carrying out this study. The present study demonstrates a computational approach of binding the interaction pattern between SeNPs and the QS signaling proteins in , utilizing multiple bioinformatics approaches. The computational investigation revealed that SeNPs were acutely 'locked' into the active region of the relevant proteins by the abundant residues in their surroundings. The PatchDock-based molecular docking analysis evidently indicated the strong and significant interaction between SeNPs and the catalytic cleft of LasI synthase (Phe105-Se = 2.7 Å and Thr121-Se = 3.8 Å), RhlI synthase (Leu102-Se = 3.7 Å and Val138-Se = 3.2 Å), transcriptional receptor protein LasR (Lys42-Se = 3.9 Å, Arg122-Se = 3.2 Å, and Glu124-Se = 3.9 Å), RhlR (Tyr43-Se = 2.9 Å, Tyr45-Se = 3.4 Å, and His61-Se = 3.5 Å), and MvfR (Leu208-Se = 3.2 Å and Arg209-Se = 4.0 Å). The production of acyl homoserine lactones (AHLs) was inhibited by the use of SeNPs, thereby preventing QS as well. Obstructing the binding affinity of transcriptional regulatory proteins may cause the suppression of LasR, RhlR, and MvfR systems to become inactive, thereby blocking the activation of QS-regulated virulence factors along with their associated gene expression. Our findings clearly showed that SeNPs have anti-QS properties against the established QS systems of , which strongly advocated that SeNPs might be a potent solution to tackle drug resistance and a viable alternative to conventional antibiotics along with being helpful in therapeutic development to cure infections.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10449602PMC
http://dx.doi.org/10.3389/fmolb.2023.1203672DOI Listing

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