title: Cytokine induction by the P. aeruginosa quorum sensing system during thermal injury.
abstract: BACKGROUND
  Pseudomonas aeruginosa causes serious infections in severely burned patients due to its ability to produce numerous virulence factors. The production of most of these factors is controlled by the cell-to-cell communication system called quorum sensing (QS). We have recently shown that several proinflammatory and hematopoietic cytokines are produced during infection of the burn wound with P. aeruginosa strain PAO1. Most of these cytokines were not produced during either thermal injury or P. aeruginosa infection alone.
  
  
  RESULTS
  In this study, we tried to determine if the QS systems play a role in the production of cytokines during P. aeruginosa infection of burn wounds. This was accomplished using the murine model of thermal injury, the P. aeruginosa strain PAO1 and its QS defective mutant (PAO-JP2), and the Multi-probe RNase protection assay. The mRNA for TNF-alpha, IL-6, TGF-beta, and G-CSF was detected within the skin of PAO1 infected/thermally injured mice. In contrast, the expression of these cytokines was not detected in PAO-JP2 infected/thermally injured mice. In comparison with the parent strain, PAO-JP2 was not defective either in its growth or in its spread within the thermally injured skin. A complementation experiment, using a plasmid that carries the intact QS gene, was conducted to confirm these results. In the presence of the complementing plasmid, PAO-JP2 produced the mRNA for the above cytokines.
  
  
  CONCLUSIONS
  These results suggest that: 1) the QS system is involved in the induction of cytokine expression during P. aeruginosa infection of burn wounds; and 2) this effect may be caused by either a component of the QS system or a QS-controlled virulence factor.
authors.affiliation: Department of Surgery, Texas Tech University Health Sciences Center, Lubbock, Texas 79430, USA.
authors.forename: Kendra P
authors.initials: KP
authors.lastname: Rumbaugh
authors.forename: Abdul N
authors.initials: AN
authors.lastname: Hamood
authors.forename: John A
authors.initials: JA
authors.lastname: Griswold
mesh_terms: D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics; D002056:Burns / Q000382:microbiology*; D002450:Cell Communication / Q000235:genetics / Q000502:physiology*; D016207:Cytokines / Q000378:metabolism*; D005260:Female; D006410:Hematopoiesis; D018836:Inflammation Mediators / Q000378:metabolism; D008025:Ligases; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation / Q000235:genetics; D010957:Plasmids / Q000235:genetics; D011552:Pseudomonas Infections / Q000503:physiopathology*; D012867:Skin / Q000293:injuries*; D014157:Transcription Factors / Q000235:genetics; D014946:Wound Infection / Q000382:microbiology*
chemical_list: D001426:Bacterial Proteins; D016207:Cytokines; D018836:Inflammation Mediators; C081237:LasI protein, Pseudomonas aeruginosa; D014157:Transcription Factors; D008025:Ligases; C096955:RHLI protein, Pseudomonas aeruginosa