re time point of jejunal segments in pig selleck lets infused with ETEC is warrant. From the results here and comparable studies, it is clear that ETEC stimulates a typical inflammatory re sponse in porcine intestinal cells, the extent of which is different according to the different ETEC strain, MOI and infection time. As mentioned above, more immune related genes which respond to F4ac ETEC or F4ab ETEC infection were detected in IPEC J2 cells than those respond to F18ac ETEC infection. It is probably due to the following reasons, Compared to F18ac ETEC, the serotypes and virulence genes of F4ab and F4ac ETEC are more similar. Adhesion ability of the three ETECs is different. At the same time point, the F4ac ETEC was the most adhesive strain, followed by F4ab ETEC with a little bit lower adhesion value, whereas F18ac ETEC showed the lowest adhesion pattern compared to F4ac ETEC and F4ab ETEC.
It has been reported that, in contrast to F4ac ETEC, F18ac ETEC has a slower colonization to the gut in vivo and it does not adhere to IPEC J2 cells nor be internalized by IPEC J2 cells in vitro. Many reports have focused on the receptor genes of ETEC F4 and F18, since they cause severe diarrhoea and edema disease in piglets. For ETEC F18, the two variants F18ab and F18ac are considered to recognize the same receptor and FUT1 is reported as the causative gene for F18 susceptibility. Up to now, a group of investigators have been searching for the ETEC F4ab F4ac receptor gene. The acknowl edged possible candidate genes include, MUC4, MUC13 and MUC20, and the latest inferred interval where the receptor gene is located is between the LMLN locus and microsatellite S0283.
In this study, the infection with F4ab ETEC Carfilzomib slightly down regulated the mRNA levels of FUT1 and MUC13 in the IPEC J2 cells, while in the F4ac ETEC infected IPEC J2 cells, the down regulated genes included, FUT1, MUC4, MUC13 and MUC20. Al though the mechanism about how ETECs infections cause down regulation of the above genes in the IPEC J2 cell line is not clear, the highly and constitutively expressed cell surface mucin MUC13 were reported to protect against intestinal inflammation in mice. We therefore suppose that intense inflammation in intestine IEC may disturb the expression of these mucin genes and further study in different time point with different MOI of ETEC is warrant.
Conclusions Gene expression profiles of the IPEC J2 cells Belinostat PXD101 with and with out F4ab, F4ac or F18ac ETEC infection were evaluated and compared. This transcriptome approach allowed us to obtain a global overview of genes and their different func tional entities involved in response to separate infection with F4ab, F4ac and F18ac ETEC specifically and or com monly. In summary, strong differential host responses to these three ETEC infections were observed. F18ac ETEC infection positively modulated the cell cycle progression and immune response of IPEC J2 cells. F4ab ETEC infec tion caused a dramatic up regulation of genes in cell cy