Contribution of flagellin subunit FliC to piglet epithelial cells invasion by F18ab E. coli.

Flagellar structures contribute to the virulence of multiple gastrointestinal pathogens either as the effectors of motility, as adhesins, or as a secretion apparatus for virulence factors. Escherichia coli F18ab variant strains are associated with edema disease (ED) in pig industries worldwide. These strains use flagella to increase the efficiency of epithelial cell invasion. In this study, we aimed to elucidate the mechanism by which flagella contribute to F18ab E. coli invasion. To explore the role of flagella in the invasion process, we performed invasion assays with either flagellated and motile, flagellated but non-motile, or non-flagellated non-motile bacteria. We observed that flagellated but non-motile bacteria invade piglet epithelial cells even more efficiently than the parent wild-type (WT) strain in vitro. By contrast, the non-flagellated bacteria have significantly reduced invasion as compared with the parent strain. These results demonstrate that flagella function mainly as adhesins to enhance the ability of F18ab E. coli to target piglet epithelial cells.