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Antimicrobial Agents and Chemotherapy, November 2009, p. 4891-4897, Vol. 53, No. 11
0066-4804/09/$08.00+0     doi:10.1128/AAC.00380-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Quorum-Quenching Acylase Reduces the Virulence of Pseudomonas aeruginosa in a Caenorhabditis elegans Infection Model{triangledown}

Evelina Papaioannou,1 Mariana Wahjudi,1,2 Pol Nadal-Jimenez,1 Gudrun Koch,1 Rita Setroikromo,1 and Wim J. Quax1*

Department of Pharmaceutical Biology, University of Groningen, 9713AV Groningen, The Netherlands,1 Faculty of Pharmacy and Faculty of Technobiology, University of Surabaya, Surabaya, Indonesia2

Received 20 March 2009/ Returned for modification 7 August 2009/ Accepted 22 August 2009

The Pseudomonas aeruginosa PAO1 gene pvdQ encodes an acyl-homoserine lactone (AHL) acylase capable of degrading N-(3-oxododecanoyl)-L-homoserine lactone by cleaving the AHL amide. PvdQ has been proven to function as a quorum quencher in vitro in a number of phenotypic assays. To address the question of whether PvdQ also shows quorum-quenching properties in vivo, an infection model based on the nematode Caenorhabditis elegans was explored. In a fast-acting paralysis assay, strain PAO1(pMEpvdQ), which overproduces PvdQ, was shown to be less virulent than the wild-type strain. More than 75% of the nematodes exposed to PAO1(pMEpvdQ) survived and continued to grow when using this strain as a food source. Interestingly, in a slow-killing assay monitoring the survival of the nematodes throughout a 4-day course, strain PAO1-{Delta}pvdQ was shown to be more virulent than the wild-type strain, confirming the role of PvdQ as a virulence-reducing agent. It was observed that larval stage 1 (L1) to L3-stage larvae benefit much more from protection by PvdQ than L4 worms. Finally, purified PvdQ protein was added to C. elegans worms infected with wild-type PAO1, and this resulted in reduced pathogenicity and increased the life span of the nematodes. From our observations we can conclude that PvdQ might be a strong candidate for antibacterial therapy against Pseudomonas infections.

* Corresponding author. Mailing address: Department of Pharmaceutical Biology, University of Groningen, 9713AV Groningen, The Netherlands. Phone: 31 (0)50 3632558. Fax: 31 (0)50 3633000. E-mail: w.j.quax{at}rug.nl

{triangledown} Published ahead of print on 31 August 2009.

Antimicrobial Agents and Chemotherapy, November 2009, p. 4891-4897, Vol. 53, No. 11
0066-4804/09/$08.00+0     doi:10.1128/AAC.00380-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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