Enterotoxigenic E. coli (ETEC) are not only a major cause of diarrhoea in travellers to and children in developing countries, but also cause neonatal and postweaning diarrhoea in piglets, leading to a reduced feed conversion and a higher mortality rate. As a consequence ETEC infections result in severe economic losses in the swine production industry. This intestinal pathogen displays colonisation factors or fimbriae on its surface enabling the microorganism to adhere to the intestinal epithelium (Fig. 1). In pig, F4 and F18 fimbriae are the most frequently associated with ETEC-induced diarrhoea1. As opposed to F4 fimbriae, oral immunisation with F18 fimbriae doesn’t protect piglets from a subsequent challenge infection2. F18 fimbriae bind glycosphingolipids in the apical membrane of enterocytes, but no transcytosis occurs, resulting in lower sunepithelial antigen concentrations as compared to F4 fimbriae, which bind the transcytotic receptor aminopeptidase N3,4. However, M-cell mediated transport of F18 fimbriae should still occur. Hence, besides a lower antigen concentration, these fimbriae could affect the function of intestinal antigen presenting cells. Here, we investigated the influence of purified F18 fimbriae on the antigen presentation capacity of small intestinal lamina propria dendritic cells (LPDCs)
