Quorum Sensing in the Gastrointestinal Tract

Abstract

This chapter reviews the published literature concerning quorum sensing (QS) among bacteria of the gastrointestinal (GI) tract, with particular emphasis on pathogenic species that cause infection in the GI tract. Three major QS circuits have been described: one used primarily by gram-negative bacteria, one used primarily by gram-positive bacteria, and one that is universal. The gram-negative bacterial QS system involves the use of acyl homoserine lactones (AHLs) as autoinducers, which then bind to response regulators that affect gene expression. The first evidence that QS could be involved in the regulation of virulence factors of GI pathogens was found with enteropathogenic E. coli (EPEC), which causes nonbloody diarrhea primarily in infants in developing countries, and enterohemorrhagic E. coli (EHEC), which causes bloody diarrhea and hemolytic-uremic syndrome. The major virulence factors for V. cholerae are cholera toxin (CT) and the toxin-coregulated pilus (TCP), both of which are regulated as part of the ToxR regulon. The discovery of QS in human pathogens has led to considerable interest in developing new therapeutic interventions to interfere with the signaling molecules. There are at least three major strategies for the development of drugs that interrupt bacterial QS: (i) inhibition of QS signal synthesis, (ii) destruction or degradation of the signal, and (iii) inhibition of signal reception. A fundamental property of QS is that the greater the density of bacteria, the greater the density of signaling molecules and the greater the opportunity for cell-to-cell communication.