Abstract
The role of flagella in the pathogenesis of F4ac+ Enterotoxigenic Escherichia coli (ETEC) mediated neonatal and post-weaning diarrhea (PWD) is not currently understood. We targeted the reference C83902 ETEC strain (O8:H19:F4ac+ LT+ STa+ STb+), to construct isogenic mutants in the fliC (encoding the major flagellin protein), motA (encoding the flagella motor), and faeG (encoding the major subunit of F4 fimbriae) genes. Both the ΔfliC and ΔfaeG mutants had a reduced ability to adhere to porcine intestinal epithelial IPEC-J2 cells. F4 fimbriae expression was significantly down-regulated after deleting fliC, which revealed that co-regulation exists between flagella and F4 fimbriae. However, there was no difference in adhesion between the ΔmotA mutant and its parent strain. These data demonstrate that both flagella and F4 fimbriae are required for efficient F4ac+ ETEC adhesion in vitro.
Highlights
Enterotoxigenic Escherichia coli (ETEC) is a major cause of diarrhea in neonatal and young pigs, causing significant economic losses, treatment costs, and reduced production efficiency
Using the undifferentiated piglet jejunum intestinal epithelial cell line IPEC-J2 as an in vitro cell model, we demonstrate that the flagellum of F4ac+ ETEC is an important virulence factor, acting in concert with F4 fimbriae, in adhering to IPEC-J2 cells in vitro
F4+ ETEC bound avidly to the IPEC-J2 cell line in vitro, which is derived from the jejunum of an un-suckled 1-day-old piglet [12]
Summary
ETEC is a major cause of diarrhea in neonatal and young pigs, causing significant economic losses, treatment costs, and reduced production efficiency. The key virulence factors of ETEC-mediated diarrhea include (i) adhesins, which mediate bacterial attachment to host enterocytes and initiate E. coli colonization and (ii) enterotoxins, which disrupt fluid homeostasis in the host small intestine and cause fluid hyper-secretion. Previous cell culture studies showed that exclusion of F4+ ETEC from attachment to epithelial cells requires repression of both the adhesin and LT [1]. As more information has been gathered, it is known that this organelle participates in many additional processes including adhesion, biofilm formation, virulence factor secretion, and the modulation of the immune system of eukaryotic cells [2,3,4,5,6].
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