Date Published: December 18, 2007
Publisher: Public Library of Science
Author(s): Steven M Opal
Abstract: Steven Opal reviews the phenomenon of bacterial communities and discusses the role played by bacterial communication and cooperation in host-pathogen interactions, particularly in urinary tract infection.
Partial Text: In this issue of PLoS Medicine, Rosen and colleagues  present convincing evidence that intracellular communities of Escherichia coli commonly exist and are likely of to be of clinical significance in uncomplicated bacterial cystitis. This novel finding is remarkable in many respects, not the least of which is the circuitous route by which our understanding about bacterial communities has evolved in the pathogenesis of infectious diseases.
This observation was initially viewed as a mere curiosity unique to marine microbiology until genome searches revealed homologous quorum sensing genes among many clinically relevant microbial pathogens [4–8]. Remarkably, many bacterial pathogens, including E. coli, use quorum sensing genes to regulate critically important virulence genes during microbial invasion.
Quorum sensing is essential to the production of healthy and fully developed biofilms. These palisade-like complex multicellular structures are relatively stable communities of bacterial populations living in a sessile, protected environment . Their slow rate of metabolism and their physical location within biofilm exopolysaccharide capsules protect bacteria against the bactericidal effect of antibiotics and host clearance by opsonins and neutrophils. A major survival advantage is gained if bacterial populations can cooperate and live in a protected, communal setting within the human host [13,14].
There are numerous implications of these findings for the pathogenesis of urinary tract infections, and for the possible treatment options available to prevent recurrent infection in UTI-prone women. These sessile bacterial communities might easily provide a sequestered site from antimicrobial defenses, allowing for repopulation of the urinary tract after a seemingly appropriate course of antimicrobial agents for bacterial cystitis. The formation of IBCs is a Toll-like receptor (TLR4)-dependent process in the murine system  and is likely to be so in humans as well. A large number of common polymorphisms exist in the TLR4 signaling apparatus in humans that affect the transcriptional rates of acute phase response genes [18–20]. What relationship exists between the frequency of IBCs, susceptibility to recurrent urinary tract infections, and human TLR4 signaling polymorphisms ?