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Escherichia coli  ( E. coli ) F17 is one of the main pathogens causing diarrhea in young livestock. The specific F17 fimbriae and lipopolysaccharide (LPS) in the surface components of  E. coli  F17 induces immune activation  via  interacting with the intestinal epithelial cells (IECs)-expressed innate immune toll-like receptors (TLRs) signaling pathway. In this study, the expression patterns of eight canonical genes from the TLR signaling pathway ( IL-6 ,  IL-8 ,  IL-1β ,  TLR4 ,  MyD88 ,  CD14 ,  TNF-α  and  TRAF6 ) were analyzed in LPS-induced IECs,  E. coli  F17-infected IECs and ileum tissue of  E. coli  F17-infected lambs. The results showed that increased expression levels of all the studied genes were observed following post-LPS-induced and  E. coli  F17-infected treatment, with  TLR4  having the highest up-regulated expression multiple (compared to NC, fold change = 17.94 and 20.11, respectively), and  CD14  having the lowest up-regulated expression multiple (fold change = 2.68 and 1.59, respectively), and higher expression levels of all the studied TLR signaling pathway genes were observed in ileum tissue of  E. coli  F17 antagonistic (AN) lambs than in  E. coli  F17 sensitive (SE) lambs. Furthermore, when compared to LPS-induced IECs,  E. coli  F17-infected IECs showed a more pronounced increase in the expression of  IL6 ,  TLR4  and  TNF-α , indicating the different roles of these genes in the IECs resistance to  E. coli  F17 infection. Our results demonstrate that the TLR signaling pathway likely promotes immune activation and provide the first evidence that TLRs have a significant potential to protect against  E. coli  F17 infections.

Expression analysis of TLR signaling pathway genes under lipopolysaccharide-induced and E. coli F17-infected sheep intestinal epithelial cells