Biofilm formation by @entity796 : role of the C4-HSL cell-to-cell signal and inhibition by XXXX .

@entity796 @entity18198 @entity4580 @entity21814 @entity21815
OBJECTIVES: In @entity796 , biofilm formation is controlled by a cell-to-cell signalling circuit relying on the secretion of @entity21814 and C4-HSL. Previous studies suggested that C4-HSL plays no significant role in biofilm formation. However the wild-type PAO1 strain PAO-BI, used as a control in these studies is itself impaired in the production of @entity21815 . We wondered therefore whether the role of C4-HSL in biofilm formation might have been underestimated, and whether @entity4580 inhibits biofilm formation by interfering with cell-to-cell signalling. METHODS: We used isogenic mutants of wild-type PAO1 strains PAO-BI and PT5 in a static biofilm model. Biofilm formation was quantified using Crystal Violet staining and exopolysaccharide measurements. RESULTS: Wild-type strain PAO-BI, as a result of its reduced C4-HSL secretion, produced 40% less biofilm compared with the wild-type PAO1 strain PT5. Using isogenic mutants of strain PT5 we have shown that whereas a lasI mutant (deficient in @entity21814 ) produced similar amounts of biofilm to the wild-type, a rhlI mutant ( @entity18198 ) produced 70% less biofilm. In the latter strain, biofilm formation could be restored by addition of exogenous C4-HSL. @entity4580 , known to reduce the production of both @entity21814 and C4-HSL, inhibited biofilm formation of wild-type PT5 by 45%. This inhibition could be reversed by the addition of both cell-to-cell signals. CONCLUSIONS: Our results indicate that C4-HSL also plays a significant role in biofilm formation. Furthermore, we demonstrate the potential of using cell-to-cell signalling blocking agents such as @entity4580 to interfere with biofilm formation.
