Abstract
Bacteria communicate extensively with each other and employ a communal approach to facilitate survival in hostile environments. A hierarchy of cell-to-cell signaling pathways regulates bacterial growth, metabolism, biofilm formation, virulence expression, and a myriad of other essential functions in bacterial populations. The notion that bacteria can signal each other and coordinate their assault patterns against susceptible hosts is now well established. These signaling networks represent a previously unrecognized survival strategy by which bacterial pathogens evade antimicrobial defenses and overwhelm the host. These quorum sensing communication signals can transgress species barriers and even kingdom barriers. Quorum sensing molecules can regulate human transcriptional programs to the advantage of the pathogen. Human stress hormones and cytokines can be detected by bacterial quorum sensing systems. By this mechanism, the pathogen can detect the physiologically stressed host, providing an opportunity to invade when the patient is most vulnerable. These rather sophisticated, microbial communication systems may prove to be a liability to pathogens as they make convenient targets for therapeutic intervention in our continuing struggle to control microbial pathogens.
Highlights
When first encountering a new host, every potential microbial pathogen is presented with three possible options
The notion that a bacterium survives essentially as a lone soldier whose success or failure is dependent upon mere happenstance alone has given way to a more complex and nuanced view of microbial pathogenesis
Up to 15% of the open reading frames of bacteria are controlled by quorum sensing (QS) molecules [4]
Summary
When first encountering a new host, every potential microbial pathogen is presented with three possible options. Many bacteria apparently do not express the luxS gene but do express the AI-2 receptor complex [17,19] Such an arrangement has been proposed to allow some bacterial strains to sense and use AI-2 signals generated by other bacteria to regulate their own coordinated transcriptional responses [6,19]. The cyclic peptide Agr system is the dominant QS regulator of genetic programs in S. aureus This major human pathogen, and other staphylococcal species, might use LuxS signals to regulate virulence and to initiate detachment from biofilms by expression of phenol-soluble modulin peptides [25,38]. In the early phase of microbial invasion, the population density is low and most virulence genes are turned off in favor of surface adherence structures and the immunoglobulin inhibitory molecule, protein A This is controlled by low agr expression and the sarA regulon of S. aureus. This process is characteristic of infection by this highly virulent, Gram-positive pathogen
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