why is quorum sensing important for biofilm formation

Cell population density-dependent regulation of gene expression is an important determinant of bacterial pathogenesis. Staphylococci have two quorum-sensing (QS) systems. The accessory gene regulator (agr) is genus specific and uses a post-translationally modified peptide as an autoinducing signal. In the pathogens Staphylococcus aureus and Staphylococcus epidermidis, agr controls the expression of a series of toxins and virulence factors and the interaction with the innate immune system. However, the role of agr during infection is controversial. A possible second QS system of staphylococci, luxS, is found in a variety of Gram-positive and Gram-negative bacteria. Importantly, unlike many QS systems described in Gram-negative bacteria, agr and luxS of staphylococci reduce rather than induce biofilm formation and virulence during biofilm-associated infection. agr enhances biofilm detachment by up-regulation of the expression of detergent-like peptides, whereas luxS reduces cell-to-cell adhesion by down-regulating expression of biofilm exopolysaccharide. Significant QS activity in staphylococci is observed for actively growing cells at a high cell density, such as during the initial stages of an infection and under optimal environmental conditions. In contrast, the metabolically quiescent biofilm mode of growth appears to be characterized by an overall low activity of the staphylococcal QS systems.

It remains to be shown whether QS control in staphylococci represents a promising target for the development of novel antibacterial agents.
Quorum-Sensing Systems, Competence, and Genetic Exchange in Biofilms Pneumococci encode several quorum-sensing (QS) systems that regulate bacterial communities to coordinate a population-type behavior and alter gene expression at very specific cell densities. The formation, maturation, and dispersal of biofilms has long been thought to be controlled or influenced by production and sensing of diffusible quorum signals. Quorum signals interact with specific receptors to regulate the expression of genes involved in bacterial competence and a number of other virulence-associated factors. Since biofilm bacteria are engaged in close contact for long periods of time, this close association increases the likelihood that quorum signaling is efficacious. As a species, S. pneumoniae is highly adaptable to changing environments, and the switch from planktonic to biofilm growth may be linked to competence gene regulation. The competence QS system produces pheromones called competence-stimulating peptides (CSPs), which facilitate bacterial competence to uptake DNA and facilitate genetic exchange in a density-dependent manner.

The functionality of the system is dependent on the gene products encoded by the comAB and comCDE genetic loci. Following a signaling cascade, not only is CSP produced, but approximately 6% of the pneumococcal genome is induced. Since only a few genes are necessary for genetic exchange, this suggests that the ComQS system plays a broader role in pneumococcal biology. The pheromone CSP may play a huge role in the promotion of pneumococcal biofilm formation and genetic exchange. CSP is encoded by the comC gene, of which many allelic variants have been identified. The most common alleles are comC1 and comC2, which produce CSP-1 and CSP-2, respectively. It is important to note that interpherotype communication does not occur. Strains can only respond to the pherotype they produce. The contribution of CSP to the planktonic and biofilm phenotypes has been recently studied. Addition of CSP increased early biofilm formation on abiotic surfaces in a comC [10,44]. Another study investigated whether CSP pherotype influenced biofilm formation; it found that clinical isolates encoding comC1 were better able to form biofilms than those encoding comC2.

Isogenic strains that expressed either the comC1 or comC2 allele were tested for their ability to form biofilms in vitro. Microscopy studies found that the comC1 variants had denser biofilms, suggesting that CSP-1 may play a more significant role in biofilm formation than CSP-2. Pneumococci have evolved and retained complex inducible autocompetence and autotransformation mechanisms that facilitate the ability to readily exchange DNA. Advantageous traits that provide a substantial survival benefit to pneumococci can be readily distributed within a biofilm community. Horizontal gene transfer (e. g. , exchange of antibiotic resistance genes) with other strains and species is a major mechanism of creating genetic and phenotypic diversity in bacterial populations. High-density pneumococcal cultures that experience reduced nutrient availability and will undergo autolysis, resulting in an increase of extracellular DNA in the environment, which can directly promote genetic exchange. Interestingly, pneumococcal strains encoding comC1. Thus, autoinduction of competence and autotransformation systems may promote horizontal gene transfer in biofilms during periods of stress and can facilitate rapid adaptation to new environmental conditions.

The Com and LuxS/autoinducer-2 (AI-2) quorum-signaling/sensing systems regulate virulence, persistence in murine carriage, and early biofilm formation on abiotic surfaces [10,26,34]. One study found that LuxS can affect early biofilm assembly on abiotic surfaces via regulation of two major virulence genes: lytA (autolysin) and ply [26,34,45]. The enzyme S -ribosylhomocysteine lyase (LuxS) produces the quorum signal homoserine lactone AI-2, a metabolic by-product of the activated methyl cycle [46,47]. Another molecule in the activated methyl cycle is S -methionine (SAM), which donates a methyl group to methionine recycling, biosynthesis of AI-2, and other reactions. Studies using quorum signal inhibitors have been successful in inhibition of biofilm formation in vitro. Sinefungin, a natural nucleoside and a structural analog of SAM, is known to have antiviral, antifungal, and antiprotozoal activities. Growth of pneumococci in the presence of sinefungin resulted in a decrease in biofilm biomass, total bacteria counts, AI-2 production, and luxS gene expression. However, there was little effect against established biofilms, suggesting this inhibitor is only effective against initial attachment and early biofilm assembly.

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