Contribution of quorum sensing to the virulence of Pseudomonas aeruginosa in pressure ulcer infection in rats

Department of Gerontological Nursing/Wound Care Management, Graduate School of Medicine, Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Wound Repair and Regeneration (Impact Factor: 2.75). 03/2011; 19(2):214-22. DOI: 10.1111/j.1524-475X.2010.00653.x
Source: PubMed


The impact of quorum sensing (QS) in in vivo models of infection has been widely investigated, but there are no descriptions for ischemic wound infection. To explore the role of QS in Pseudomonas aeruginosa in the establishment of ischemic wound infection, we challenged a pressure ulcer model in rats with the PAO-1, PAO-1 derivatives ΔlasIΔrhlI and ΔlasRΔrhlR strains, which cannot induce the virulence factor under QS control, thus the reduced tissue destruction was expended in these mutant strains. However unexpectedly, on postwounding day 3, the inflammatory responses in the three groups were similarly severe and the numbers of bacteria in tissue samples did not differ among the three strains. Biofilm formation was immature in QS-deficient strains, defined by the absence of dense bacterial aggregates and extracellular polymeric substance, which was confirmed by scanning electron microscopy. The Pseudomonas aeruginosa QS signal, acylated homoserine lactone, was only quantified from wound samples in the PAO-1 group. The swimming and twitching motilities were significantly enhanced in the ΔlasRΔrhlR group compared with the PAO-1 group in vitro. A significantly larger wound area was correlated with the bacterial motility. The inflammation in the early phase of bacterial challenge to wounds with immature biofilm formation in the QS-deficient strains indicated that the role of QS was more crucial for the chronic phase than for the acute phase of infection. The present findings indicate a difference in the importance of QS in ischemic wound infections compared with other infection models.

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    • "Our study has also shown the lack of Pseudomonas virulence factors and genes for QS molecules within wound isolates, which goes in line with previous studies [64] confirming that spontaneous QS- and virulence-deficient P. aeruginosa mutants are still capable of causing wound infections. Pseudomonas has two QS systems, LasI-LasR and RhlI-RhlR, shown to be important for wound infection and biofilm formation in rodent models [32], [36]. Although we analyzed a small number of isolates, the lack of LasI in some and the presence of RhlI in all of the tested strains suggest that RhlI might be more important than LasI for cutaneous wound infections. "
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