Abstract
Enterotoxigenic Escherichia coli (ETEC) F4ac is a major constraint to the development of the pig industry, which is causing newborn and post-weaning piglets diarrhea. Previous studies proved that FaeG is the major fimbrial subunit of F4ac E. coli and efficient for bacterial adherence and receptor recognition. Here we show that the faeG deletion attenuates both the clinical symptoms of F4ac infection and the F4ac-induced intestinal mucosal damage in piglets. Antibody microarray analysis and the detection of mRNA expression using porcine neonatal jejunal IPEC-J2 cells also determined that the absence of FaeG subunit alleviated the F4ac promoted apoptosis in the intestinal epithelial cells. Thus, targeted depletion of FaeG is still beneficial for the prevention or treatment of F4ac infection.
Highlights
Enterotoxigenic Escherichia coli (ETEC) F4 is the leading cause of diarrhea in neonatal and post-weaning piglets (Sugiharto et al 2012; Van den Broeck et al 2002)
Our previous study has shown that FaeG mediates the binding of F4ac E. coli with both porcine brush border cells and IPEC-J2 cells and interacts with the receptor of F4 fimbriae directly (Xia et al 2016, 2015b)
Enzymatic activities of caspase-3, -8 and -9 were measured in IPEC-J2 cells from both noninfected and bacterial infected groups (Fig. 3c), and the Discussion As the initial step for ETEC F4 infection, bacterial attachment to intestinal epithelial cell (IEC) and the interaction between fimbriae and the specific receptor of the host are both crucial for the development of disease
Summary
Enterotoxigenic Escherichia coli (ETEC) F4 is the leading cause of diarrhea in neonatal and post-weaning piglets (Sugiharto et al 2012; Van den Broeck et al 2002). The bacteria induce the disease depending on the interaction between fimbriae and host receptors, while fimbriaemediated attachment to the intestinal epithelium is the initial step in these infections (Xia et al 2015b). Among these three fimbrial variants, i.e., F4ab, F4ac, and F4ad, F4ac is the most common serotype and FaeG is the major subunit of F4 fimbriae (Sugiharto et al 2012; Van den Broeck et al 2002). Our previous study has shown that FaeG mediates the binding of F4ac E. coli with both porcine brush border cells and IPEC-J2 cells and interacts with the receptor of F4 fimbriae directly (Xia et al 2016, 2015b).
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