The status of population density is communicated among bacteria by specific secreted molecules, called
pheromones or autoinducers, and the control mechanism is called ""quorum-sensing"". Quorum-sensing systems regulate the expression of a panel of genes, allowing bacteria to adapt to modified environmental conditions at a high density of population. The two known different quorum systems are described as the LuxR-LuxI system in gram-negative bacteria, which uses an N-
acyl-homoserine lactone (AHL) as signal, and the agr system in gram-positive bacteria, which uses a
peptide-tiolactone as signal and the
RNAIII as effector molecules. Both in gram-negative and in gram-positive bacteria, quorum-sensing systems regulate the expression of adhesion mechanisms (biofilm and adhesins) and
virulence factors (toxins and exoenzymes) depending on population cell density. In gram-negative Pseudomonas aeruginosa, analogs of signaling molecules such as furanone analogs, are effective in attenuating bacterial virulence and controlling
bacterial infections. In grampositive Staphylococcus aureus, the quorum-sensing
RNAIII-inhibiting peptide (RIP), tested in vitro and in animal
infection models, has been proved to inhibit virulence and prevent
infections. Attenuation of bacterial virulence by quorum-sensing inhibitors, rather than by bactericidal or bacteriostatic drugs, is a highly attractive concept because these
antibacterial agents are less likely to induce the development of bacterial resistance.