Inactivation of the rhlA gene in Pseudomonas aeruginosa prevents rhamnolipid production, disabling the protection against polymorphonuclear leukocytes

@article{vanGennip2009InactivationOT,
  title={Inactivation of the rhlA gene in Pseudomonas aeruginosa prevents rhamnolipid production, disabling the protection against polymorphonuclear leukocytes},
  author={Maria van Gennip and Louise Dahl Christensen and Morten Alhede and Richard Kerry Phipps and Peter {\O}strup Jensen and Lars Jackie Christophersen and S{\"u}nje Johanna Pamp and Claus E Moser and Per Jensen Mikkelsen and Andrew Y. Koh and Tim Tolker-Nielsen and Gerald B. Pier and Niels H{\O}iby and Michael Givskov and Thomas Bjarnsholt},
  journal={APMIS},
  year={2009},
  volume={117}
}
Many of the virulence factors produced by the opportunistic human pathogen Pseudomonas aeruginosa are quorum‐sensing (QS) regulated. Among these are rhamnolipids, which have been shown to cause lysis of several cellular components of the human immune system, e.g. monocyte‐derived macrophages and polymorphonuclear leukocytes (PMNs). We have previously shown that rhamnolipids produced by P. aeruginosa cause necrotic death of PMNs in vitro. This raises the possibility that rhamnolipids may… 

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References

SHOWING 1-10 OF 45 REFERENCES

Rapid necrotic killing of polymorphonuclear leukocytes is caused by quorum-sensing-controlled production of rhamnolipid by Pseudomonas aeruginosa.

TLDR
The results demonstrate the potential of the QS system to facilitate infections with P. aeruginosa by disabling the PMNs, which are a major first line of defence of the host.

Effects of Pseudomonas aeruginosa rhamnolipids on human monocyte‐derived macrophages

TLDR
A simplified method for the isolation of these rhamnolipids is described and the possible significance of these extracellular bacterial glycolipids as a virulence factor in the pathogenesis of P. aeruginosa is discussed.

Impact of Pseudomonas aeruginosa quorum sensing on biofilm persistence in an in vivo intraperitoneal foreign-body infection model.

TLDR
The present results support a model by which functional QS systems play a pivotal role in the ability of bacteria to resist clearing by the innate immune system and strongly suggest that the efficiency of the mouse innate defence against biofilm-forming P. aeruginosa is improved when the bacteria are treated with QS drugs that induce QS deficiency.

Rhamnolipid Surfactant Production Affects Biofilm Architecture in Pseudomonas aeruginosa PAO1

TLDR
It is proposed that the maintenance of biofilm architecture represents a previously unrecognized step in the development of these microbial communities, and evidence that surfactants may be able to maintain open channels by affecting cell-cell interactions and the attachment of bacterial cells to surfaces is provided.

Attenuation of Pseudomonas aeruginosa virulence by quorum sensing inhibitors

TLDR
A synthetic derivate of natural furanone compounds can act as a potent antagonist of bacterial quorum sensing and inhibited virulence factor expression in a mouse pulmonary infection model.

A second N-acylhomoserine lactone signal produced by Pseudomonas aeruginosa.

TLDR
The role of factor 2 in virulence gene regulation remains to be determined, but this compound may affect the expression of lasR, which in turn activation of numerous virulence genes in the presence of sufficient PAI.

Overexpression of the MexEF-OprN Multidrug Efflux System Affects Cell-to-Cell Signaling in Pseudomonas aeruginosa

TLDR
It is reported that nfxC type mutants, overexpressing the MexEF-OprN efflux system, produce lower levels of extracellular virulence factors than the susceptible wild type.

Multiple Roles of Biosurfactants in Structural Biofilm Development by Pseudomonas aeruginosa

TLDR
Genetic evidence is presented that during biofilm development by P. aeruginosa, biosurfactants promote microcolony formation in the initial phase and facilitate migration-dependent structural development in the later phase of biofilm formation.

Transcriptome analysis of Pseudomonas aeruginosa biofilm development: anaerobic respiration and iron limitation

TLDR
This study shows that, when compared with planktonic bacteria, gene expression profiles of biofilm cells have the highest resemblance to the profiles of stationary-phase cells, and presents evidence that quorum sensing is participating in the control of iron-limitation responses in theBiofilm cells.

Microbial pathogenesis in cystic fibrosis: mucoid Pseudomonas aeruginosa and Burkholderia cepacia.

TLDR
This review summarizes the latest advances in understanding host-pathogen interactions in CF with an emphasis on the role and control of conversion to mucoidy in P. aeruginosa and B. cepacia.