The antibacterial effect of lactoferrin on porcine enterotoxigenic E. coli
Authors & affiliation
s:Dierick M
1., Vanrompay D.
2, Devriendt B.
1, Cox E
1.
1 Laboratory of Immunology, Faculty of Veterinary Medicine, UGent
2 Department of Molecular Biotechnology, Faculty of Bioscience Engineering, UGent
Introduction: F4- and F18-fimbriated E. coli infections cause postweaning diarrhoea in piglets. This results in morbidity and a decreased quality of life of the piglets. Moreover, there are severe economic losses for the pig industry due to diarrhoea, growth retardation, mortality and elevated use of medicines. Extensive use of antibiotics and zinc oxide during the first two weeks after weaning is used to control post-weaning diarrhoea and has most likely contributed to an increased occurrence of antibiotic resistant strains. Naturally derived antimicrobials agents have been proposed as possible alternatives. One of these alternatives is lactoferrin, as it is known to posses several antimicrobial and immune modulatory properties.
Aims: To evaluate the antibacterial effect, such as proteolytic activity, bacterial growth inhibition and adhesion, of different lactoferrins in order to implement lactoferrin as a novel strategy to improve gut health during the postweaning period in piglets.
Results: We have analysed the ability of several lactoferrins, such as bovine lactoferrin, porcine lactoferrin and ovotransferrin, to inhibit the growth of porcine enterotoxigenic E. coli (ETEC), to degrade ETEC-derived colonisation factors and to inhibit the adherence of ETEC to porcine intestinal epithelial cells. Our results revealed that bovine lactoferrin and porcine lactoferrin, but not ovotransferrin, inhibit the growth of an F4-fimbriated ETEC strain. Furthermore, bovine lactoferrin, porcine lactoferrin and ovotransferrin, which are known to have serine protease activity, were shown to degrade F18 fimbriae. Additionally, bovine lactoferrin and porcine lactoferrin were also able to degrade F4 fimbriae. The capacity of lactoferrin to degrade these fimbriae might be essential in the inhibition of bacterial adhesion to host cells. In an in vitro cell attachment assay, we showed that bovine lactoferrin, ovotransferrin and porcine lactoferrin can decrease the number of adherent bacteria to porcine intestinal epithelial cells. Furthermore, we have shown that this decrease in adhesion is dependent on the proteolytic activity of lactoferrin.
Conclusions: Our findings demonstrate that lactoferrin can directly affect porcine ETEC strains, showing that lactoferrin holds promise to prevent ETEC infections in piglets and reduce antimicrobial use.
