Correction to “<i>N</i>-Acyl <scp>l</scp>-Homocysteine Thiolactones Are Potent and Stable Synthetic Modulators of the RhlR Quorum Sensing Receptor in <i>Pseudomonas aeruginosa</i>”

Boursier, Michelle E.; Combs, Joshua B.; Blackwell, Helen E.

doi:10.1021/acschembio.0c00331

Cited by 1 publication

(2 citation statements)

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“…Two AHL-mediated QS systems are found in P. aeruginosa , which consist of the Lux homologs LasRI and RhlRI. Two LuxI-type synthases, LasI and RhlI, produce 3OC12-HSL and C4-HSL, respectively (Boursier et al., 2020 ; Høyland-Kroghsbo et al., 2017 ; Soukarieh et al., 2018 ). These two signaling molecules are recognized by their cognate LuxR-type receptors, LasR and RhlR, and subsequently activate the expression of QS target genes (Boursier et al., 2020 ; Fong et al., 2018 ; O'Loughlin et al., 2013 ).…”

Section: Introductionmentioning

confidence: 99%

“…Two LuxI-type synthases, LasI and RhlI, produce 3OC12-HSL and C4-HSL, respectively (Boursier et al., 2020 ; Høyland-Kroghsbo et al., 2017 ; Soukarieh et al., 2018 ). These two signaling molecules are recognized by their cognate LuxR-type receptors, LasR and RhlR, and subsequently activate the expression of QS target genes (Boursier et al., 2020 ; Fong et al., 2018 ; O'Loughlin et al., 2013 ). In P. aeruginosa , swarming motility, biofilm maturation, and the expression of virulence factors such as exoproteases, hemolysins, exotoxin A, exoenzyme S, pyocyanin, cyanide, and the cytotoxic lectins PA-IL and PA-IIL are controlled by QS (Ahmed et al., 2021 ; Luo et al., 2017 ; Passador et al., 1993 ).…”

Section: Introductionmentioning

confidence: 99%

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Reducing the virulence of Pseudomonas aeruginosa by using multiple quorum-quenching enzymes

Khatun,

Hoque,

Koffas

et al. 2023

Journal of Industrial Microbiology and Biotechnology

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The emergence of multidrug-resistant Pseudomonas aeruginosa in healthcare settings poses a tremendous challenge to traditional antibiotic therapy. P. aeruginosa utilizes quorum sensing (QS) to coordinate the production of virulence factors and the formation of drug-resistant biofilms. QS is mediated by signal compounds produced by P. aeruginosa as well as signal molecules produced by other non-pseudomonad bacteria. A potential strategy to prevent bacterial pathogenicity is utilizing enzymes to interfere with QS. Here, we used AidC, a quorum-quenching enzyme from Chryseobacterium sp. strain StRB126 that can effectively hydrolyze N-(3-oxododecanoyl) homoserine lactone (3OC12-HSL) and N-butanoyl-homoserine lactone (C4-HSL), the major signal molecules synthesized by P. aeruginosa. The exogenous addition of AidC to P. aeruginosa wild-type strain PAO1 cultures significantly reduced the total protease and elastase activities and the production of pyocyanin. In addition, the application of AidC resulted in thin and sparse biofilm formation. Later, we used a metagenomic-derived quorum quenching (QQ) enzyme QQ-2 in combination with AidC to attenuate PAO1 virulence when the presence of a non-pseudomonad signal compound AI-2 aggravated it. These findings suggest that using a combined antimicrobial approach may lead to a more efficacious therapeutic intervention against P. aeruginosa PAO1 infection, as its behavior is modulated in the presence of intraspecies and interspecies signal compounds.

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