Bacterial flagella contribute to pathogen virulence; however, the role of flagella in the pathogenesis of F18ab E. coli-mediated swine edema disease (ED) is not currently known. We therefore evaluated the role of flagella in F18ab E. coli adhesion, invasion, biofilm formation, and IL-8 production using an in vitro cell infection model approach with gene-deletion mutant and complemented bacterial strains. We demonstrated that the flagellin-deficient fliC mutant had a marked decrease in the ability to adhere to and invade porcine epithelial IPEC-J2 cells. Surprisingly, there was no difference in adhesion between the F18 fimbriae-deficient Δ. fedA mutant and its parent strain. In addition, both the Δ. fedA and double Δ. fliCΔ. fedA mutants exhibited an increased ability to invade IPEC-J2 cells compared to the wild-type strain, although this may be due to increased expression of other adhesins following the loss of F18ab fimbriae and flagella. Compared to the wild-type strain, the Δ. fliC mutant showed significantly reduced ability to form biofilm, whereas the Δ. fedA mutant increased biofilm formation. Although Δ. fliC, Δ. fedA, and Δ. fliCΔ. fedA mutants had a reduced ability to stimulate IL-8 production from infected Caco-2 cells, the Δ. fliC mutant impaired this ability to a greater extent than the Δ. fedA mutant. The results from this study clearly demonstrate that flagella are required for efficient F18ab E. coli adhesion, invasion, biofilm formation, and IL-8 production in vitro.
- F18ab E. coli
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