Bacteria can attach to surfaces and form communities enmeshed
in a self-produced polymeric matrix, which can consist of protein,
polysaccharide, and nucleic acid. These communities comprise
a biofilm [6,7]. When P. aeruginosa chronically infects patients it
adapts to the biofilm mode of growth. For example, the persistence
of P. aeruginosa in the lungs of cystic fibrosis patients has been
linked, in part, to its ability to form biofilms [8,9]. Destruction of
established biofilm is one of the most challenging problems in
treating chronic P. aeruginosa infections [6]. Once this structure
forms, the colony is protected from the patient’s immune system
and is less susceptible to drug treatments. Effective biofilm inhibitors
could dramatically improve treatment regimens for many
infectious diseases and benefit large patient populations.
P. aeruginosa produces a wide range of virulence factors that are
regulated by a cell-to-cell signaling mechanism known as quorum
sensing (QS). QS was first discovered as a mechanism to control the
luminescence of Vibrio fischeri, a bacterium that forms a mutualistic
light organ symbiosis with certain marine animals [10,11]. Bacteria
that use QS produce and secrete certain signaling compounds
(called autoinducers, AI) to signal each other and to coordinate
their activities. For example, gram-positive bacteria use small