Quorum Sensing System Lactones Do Not Increase Invasiveness of a MexAB‐OprM Efflux Mutant but Do Play a Partial Role in Pseudomonas aeruginosa Invasion

We studied the quorum sensing (QS) system and the related homoserine lactones (HSLs) observing Pseudomonas aeruginosa invasion using the epithelial cell monolayer penetration assay model. Compared to the PAO1 wild‐type, the QS mutants, ΔlasI and ΔrhlI, were compromised in their capacity to invade. The decreased invasiveness of ΔrhlI was restored by adding 100 μM exogenous C4‐HSL. However, the decreased invasiveness of an efflux mutant, AmexAB‐oprM, was not restored in the presence of exogenous HSLs. The QS system partially plays a role in P. aeruginosa invasion; however, C4‐HSL and 3‐O‐C12‐HSL are not the essential determinants for invasiveness for P. aeruginosa.

[1]  J. Daurès,et al.  Risk factors for multidrug-resistant Pseudomonas aeruginosa nosocomial infection. , 2004, The Journal of hospital infection.

[2]  T. Nakae,et al.  Enhancement of the mexAB-oprM Efflux Pump Expression by a Quorum-Sensing Autoinducer and Its Cancellation by a Regulator, MexT, of the mexEF-oprN Efflux Pump Operon in Pseudomonas aeruginosa , 2004, Antimicrobial Agents and Chemotherapy.

[3]  H. Schweizer.  Efflux as a mechanism of resistance to antimicrobials in Pseudomonas aeruginosa and related bacteria: unanswered questions. , 2003, Genetics and molecular research : GMR.

[4]  R. Hancock,et al.  Multidrug Efflux Systems Play an Important Role in the Invasiveness of Pseudomonas aeruginosa , 2002, The Journal of experimental medicine.

[5]  T. A. Springer,et al.  IL-8 Production in Human Lung Fibroblasts and Epithelial Cells Activated by the Pseudomonas Autoinducer N-3-Oxododecanoyl Homoserine Lactone Is Transcriptionally Regulated by NF-κB and Activator Protein-21 , 2001, The Journal of Immunology.

[6]  K. Poole,et al.  Multidrug efflux pumps and antimicrobial resistance in Pseudomonas aeruginosa and related organisms. , 2001, Journal of molecular microbiology and biotechnology.

[7]  N. Masuda,et al.  Contribution of the MexX-MexY-OprM Efflux System to Intrinsic Resistance in Pseudomonas aeruginosa , 2000, Antimicrobial Agents and Chemotherapy.

[8]  B. Finlay,et al.  Penetration of clinical isolates of Pseudomonas aeruginosa through MDCK epithelial cell monolayers. , 2000, The Journal of infectious diseases.

[9]  R. Gaynes,et al.  Nosocomial infections in medical intensive care units in the United States. National Nosocomial Infections Surveillance System. , 1999, Critical care medicine.

[10]  K. Poole,et al.  Influence of the MexAB-OprM Multidrug Efflux System on Quorum Sensing in Pseudomonas aeruginosa , 1998, Journal of bacteriology.

[11]  M. Tsuda,et al.  Characterization of the MexC-MexD-OprJ Multidrug Efflux System in ΔmexA-mexB-oprM Mutants of Pseudomonas aeruginosa , 1998, Antimicrobial Agents and Chemotherapy.

[12]  Yasuaki Yamada,et al.  Adherence to and Penetration of Human Intestinal Caco-2 Epithelial Cell Monolayers by Pseudomonas aeruginosa , 1998, Infection and Immunity.

[13]  B. Iglewski,et al.  Roles of Pseudomonas aeruginosa las and rhl quorum-sensing systems in control of elastase and rhamnolipid biosynthesis genes , 1997, Journal of bacteriology.

[14]  M. Plotkowski,et al.  Asialo GM1 is a receptor for Pseudomonas aeruginosa adherence to regenerating respiratory epithelial cells , 1996, Infection and immunity.

[15]  E. Greenberg,et al.  A second N-acylhomoserine lactone signal produced by Pseudomonas aeruginosa. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[16]  E. Greenberg,et al.  Structure of the autoinducer required for expression of Pseudomonas aeruginosa virulence genes. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[17]  M. Gambello,et al.  Expression of Pseudomonas aeruginosa virulence genes requires cell-to-cell communication. , 1993, Science.

[18]  R. Baltimore,et al.  Immunohistopathologic localization of Pseudomonas aeruginosa in lungs from patients with cystic fibrosis. Implications for the pathogenesis of progressive lung deterioration. , 1989, The American review of respiratory disease.

[19]  G. Dougan,et al.  Identification and characterization of TnphoA mutants of Salmonella that are unable to pass through a polarized MDCK epithelial cell monolayer , 1988, Molecular microbiology.

[20]  B. Finlay,et al.  Penetration of Salmonella through a polarized Madin-Darby canine kidney epithelial cell monolayer , 1988, The Journal of cell biology.

[21]  G. Campbell,et al.  Phenotypic comparison of Pseudomonas aeruginosa strains isolated from a variety of clinical sites , 1986, Journal of clinical microbiology.