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biofilms live in a microhabitat that has primitive homeostasis, a primitive circulatory system,
and metabolic cooperativity, and which provides protection against changes in the
surrounding milieu. Biofilms are hence paradigm examples of complex communities where
QS and cross-talk can have a strong influence [Stanley and Lazazzera, 2004].
Biofilms are a major concern for human activities. Biofilm bacteria have detrimental
effects on industrial installations, being involved in biofouling of water systems, microbially-
induced corrosion of pipes and tanks, degradation of stored industrial products, spoilage of
processed foods and pharmaceutical drugs [Pasmore and Costerton, 2003, Coetser and Cloete,
2005]. The pathogenesis of infections associated with many medical devices is also related to
microorganisms growing in biofilms. Biomaterials that are most likely to be compromised by
biofilm associated infections are urethral or intravascular catheters and implants (i.e. joint
prostheses, intraocular lenses, artificial heart valves, stents) [Costerton et al. , 2005, Ha and
Cho, 2006]. Biofilm formation in such devices greatly hampers eradication of the involved
flora by antibiotics, as diffusion inside the biofilm structure is limited, making them highly
resistant to treatment, which makes them a reservoir for bacterial contamination. Besides,
within the high dense bacterial population, resistance and virulence genes are very efficiently
transferred [Costerton et al. , 2005].
As already summarized in Table 1., the formation of bacterial biofilms is commonly
regulated by QS mechanisms. The QS system of the opportunistic pathogen Pseudomonas
aeruginosa has been thoroughly analyzed (reviewed by de Kievit and Iglewsky, 2000,
Bjarnsholt and Givskov, 2007]. P. aeruginosa mutants defective in AHL production form
biofilms with altered morphology and characteristics, compared to wild type strains. Biofilm
formation by P. aeruginosa , involves the expression of a wide number of genes, and the
whole process is regulated by the lasR and lasI genes by means of a single AHL (3-oxo-C 12 -
HSL). However, there are complex interactions of the 3-oxo-C 12 -HSL-based QS system with
other QS signals (a second AHL-producing locus, PQS, and diketopiperazins, see Figure 1)
[de Kievit and Iglewsky, 2000].
Many other human pathogens causing bacteraemia, meningitis, and a variety of oral,
gastrointestinal, and cutaneous infections communicate by QS mechanisms, either under the
control of AHLs, AIPs or AI-2 based systems (reviewed by Donabedian, 2003, Vendeville et
al. , 2005). Cell density not only influences biofilm formation on invaded tissues, but also
regulates important events during the infection process, such as the synthesis and secretion of
virulence factors (Table 1). Recent research has lead to the proposal that interference with this
communication system offers potential targets for the design of novel antimicrobial drugs. In
the future, treatments that inhibit the transcription of biofilm control genes or attenuate
bacterial pathogenicity (rather than inhibit bacterial growth) might provide a successful
strategy for the inhibition of infections [Pasmore and Costerton, 2003, Bjarnsholt and
Givskov, 2007]. Drugs directed to blocking of QS will not exert selective pressure and hence
resistances are less likely to arise [Vendeville et al. , 2005]. The introduction of QS signal
blockers in anti-infectious therapy is a very attractive new approach, as it will provide a
particularly useful tool against strains of bacteria exhibiting multi-resistance to conventional
antibiotics.
7.3. Quorum Quenching
As already pointed out in Section 6., some organisms synthesize compounds which
interfere with the bacterial QS communication systems. In the case of pathogenic bacterial-
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