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It is now well established that a number of bacteria communicate through diffusible signals that may induce and/or regulate a coordinated response by the individual organisms that make up a given population or biofilm. For many of these organisms, it has been suggested that intercellular signaling functions to report population density or to coordinate a response from all cells in a microbial community. Therefore, cell-to-cell communication has been referred to as auto-induction or quorum sensing. The response of bacteria to quorum sensing signals is quite varied and includes, for example, the induction of bioluminescence, the regulation of virulence gene expression, the formation of biofilms, or the induction of horizontal transfer of genetic material. It is also becoming increasingly apparent that some bacteria may communicate via contact-dependent signaling mechanisms, and that the response to direct cell-to-cell contact influences complex behaviors that may contribute to multicellular development or the adaptation to growth in complex biofilms. In the past five to ten years, increased interest and research in the mechanisms of bacterial cell-to-cell communication has revealed surprising complexity both in the signaling processes themselves and in the breadth of the response of recipient cells to the signal molecules. For example, a variety of chemical species, e.g. acyl-homoserine lactones, oligopeptides, furan derivatives (i.e. AI-2), quinolones, butyrolactones, and unsaturated fatty acids are known or have been suggested to function as diffusible signals. Furthermore, some organisms, most notably Pseudomonas aeruginosa and species of Vibrio, have been shown to produce and respond to multiple diffusible signal molecules.
Many bacterial diseases are caused by organisms growing together as communities or biofilms. These microorganisms have the capacity to coordinately regulate specific sets of genes by sensing and communicating amongst themselves utilizing a variety of signals. This book examines the mechanisms of quorum sensing and cell-to-cell communication in bacteria and the roles that these processes play in regulating virulence, bacterial interactions with host tissues, and microbial development. Recent studies suggest that microbial cell-to-cell communication plays an important role in the pathogenesis of a variety of disease processes. Furthermore, some bacterial signal molecules may possess immunomodulatory activity. Thus, understanding the mechanisms and outcomes of bacterial cell-to-cell communication has important implications for appreciating host-pathogen interactions and ultimately may provide new targets for antimicrobial therapies that block or interfere with these communication networks.
The microbial community that exists in the oral cavity is perhaps the most accessible, complex and pathogenic of the naturally occurring human biofilms. Over 500 different species of bacteria have been identified in the mature biofilm that forms on tooth surfaces (38). This complex community tenaciously adheres to and develops on the acquired salivary pellicle, a conditioning film of salivary proteins and glycoproteins adsorbed to oral tissue surfaces. The initial colonizers of the salivary pellicle are predominantly Gram-positive facultative anaerobes such as the streptococci; these organisms normally exist in commensal harmony with the host. However, as the oral biofilm matures, there is a change in the microbial composition, with an increasing presence of Gram-negative organisms. The two most common oral diseases in humans, dental caries and periodontal disease, arise from populational shifts in the biofilm in response to a variety of host and/or environmental stimuli. This results in over-representation of pathogenic organisms in the biofilm at afflicted sites in the oral cavity. For example, excessive consumption of dietary sucrose favors the overgrowth of highly fermentative acidophilic organisms such as Streptococcus mutans. The acidic local environment generated by these organisms promotes demineralization of the hydroxyapatite matrix of enamel, thus increasing the risk of dental caries. In contrast, periodontal disease is caused by a biofilm that thrives in the subgingival pocket and induces a chronic inflammatory condition that results in the destruction of the connective tissues and bone that support the teeth (23).