Porcine and bovine lactoferrin inhibit growth of porcine enterotoxigenic E. coli and degrades their virulence factors.

Post-weaning diarrhoea (PWD) is an economically important, multifactorial disease affecting pigs within the first two weeks after weaning. The most common agent associated with PWD is enterotoxigenic E. coli (ETEC). Currently, antibiotics are used to control PWD and this has most likely contributed to an increased prevalence of antibiotic resistant strains. This puts pressure on veterinarians and farmers to decrease or even abandon the use of antibiotics, but these measures need to be supported by alternative strategies for controlling these infections. Natural derived molecules, such as lactoferrin, could be potential candidates due to their antibacterial or immune modulating activities. Here, we analyzed the ability of bovine lactoferrin (bLF), porcine lactoferrin (pLF) and ovotransferrin (ovoTF) to inhibit ETEC growth, degrade ETEC virulence factors and inhibit adherence of these pathogens to porcine intestinal epithelial cells. Our results revealed that bLF and pLF, but not ovoTF, inhibit the growth of ETEC. Furthermore, bLF and pLF can degrade several virulence factors produced by ETEC strains, more specifically F4 fimbriae, F18 fimbriae and flagellin. On the other hand, ovoTF is able to degrade F18 fimbriae and flagellin, but not F4 fimbriae. An in vitro adhesion assay showed that bLF, ovoTF and pLF can decrease the number of adherent bacteria to epithelial cells. Our findings demonstrate that lactoferrin can directly affect porcine ETEC strains, which could allow lactoferrin to serve as alternative for antimicrobials to prevent ETEC infections in piglets. IMPORTANCE Currently, post-weaning F4+ and F18+E. coli infections in piglets are controlled by the use of antibiotics and zinc-oxide, but the use of these antimicrobial agents most likely contributes to the increase in antibiotic resistance. Our work demonstrates that bovine and porcine lactoferrin can inhibit the bacterial growth of porcine enterotoxigenic E. coli strains. In addition, we also show that lactoferrin can reduce the adherence of these strains to small intestinal epithelial cells, even at a concentration that does not inhibit bacterial growth. This research could allow us to develop lactoferrin as an alternative strategy to prevent ETEC infections in piglets.