Abstract
Chemical communication mediates signaling between cells. Bacteria also engage in chemical signaling, termed quorum sensing (QS), to coordinate population-wide behavior. The bacterial pathogen enterohemorrhagic E. coli (EHEC), responsible for outbreaks of bloody diarrhea worldwide, exploits QS to promote expression of virulence factors in humans. Although EHEC is a human pathogen, it is a member of the gastrointestinal (GI) flora in cattle, the main reservoir for this bacterium. EHEC cattle colonization requires SdiA, a QS transcription factor that uses acyl-homoserine lactones (AHLs), for proper folding and function. EHEC harbors SdiA, but does not produce AHLs, consequently having to sense AHLs produced by other bacterial species. We recently showed that SdiA is necessary for efficient EHEC passage through the bovine GI tract, and show that AHLs are prominent within cattle rumen, but absent from the other sections of the GI tract. EHEC utilizes the locus of enterocyte effacement (LEE) to colonize the recto-anal junction of cattle, and the glutamate decarboxylase (gad) system to colonize cows. Transcription of the LEE genes is decreased by rumen AHLs through SdiA, while transcription of the gad acid resistant system is increased. It would be expensive for EHEC to express the LEE genes in the rumen where they are not necessary. However, in preparation for the acidic distal stomachs the EHEC gad is activated in the rumen. Hence AHL signaling through SdiA aids EHEC in gauging these environments, and modulates gene expression towards adaptation to a commensal life-style in cattle.1 Inasmuch as EHEC is largely prevalent in cattle herds, interference with SdiA-mediated QS inhibition of cattle colonization could be an attractive approach to diminish contamination of food products due to cattle shedding of this pathogen.