PchE Regulation of O157:H7 Flagella, Controlling the Transition to Host Cell Attachment.

Shiga toxins and intimate adhesion controlled by the locus of enterocyte effacement are major enterohemorrhagic (EHEC) virulence factors. Curli fimbriae also contribute to cell adhesion and are essential biofilm components. The transcriptional regulator PchE represses the expression of curli and their adhesion to HEp-2 cells. Past studies indicate that also represses additional adhesins that contribute to HEp-2 cell attachment. In this study, we tested for regulation of several tissue adhesins and their regulators. Three adhesin-encoding genes (, , ) and four master regulators (, , , ) were controlled by . over-expression strongly up-regulated but the marked flagella induction reduced the attachment of O157:H7 clinical isolate PA20 to HEp-2 cells, indicating that flagella were blocking cell attachments rather than functioning as an adhesin. Chemotaxis, motor, structural, and regulatory genes in the flagellar operons were all increased by expression, as was PA20 motility. This study identifies new members in the regulon and shows that stimulates flagellar motility while repressing cell adhesion, likely to support EHEC movement to the intestinal surface early in infection. However, induced or inappropriate -dependent flagellar expression could block cell attachments later during disease progression.