Bovine colostrum increases the viability and the healing process of IPEC-J2 intestinal porcine epithelial cells while modulating the barrier function and Escherichia coli-mediated inflammatory responses

Piglet gut response to weaning results in impaired intestinal barrier function, increased inflammatory response and susceptibility to enteric diseases. As the use of antibiotics as growth promoters will be restricted in the swine industry in Canada, novel feeding strategies to improve gut health are needed. This study aims to determine the potential of defatted bovine colostrum (BC) and its fractions, the serocolostrum (SC) and caseins (CAS), to promote viability and the healing process and to modulate barrier integrity and the inflammatory response induced by enterotoxigenic E. coli (ETEC) in IPEC-J2 intestinal epithelial porcine cells. To evaluate cell viability and wound healing, XTT cell proliferation and migration scratch assays were performed on IPEC-J2 cells incubated with BC, SC, or CAS. Monolayer permeability of ETEC infected IPEC-J2 cells incubated with BC, SC or CAS was monitored by transepithelial electrical resistance measurements. Inflammatory and oxidative responses were assessed by gene expression analysis of several cytokines and chemokines by qPCR. Incubation with BC derivatives led to 8 to 14% increases IPEC-J2 cell viability, in comparison to untreated cells (P ≤ 0.05). IPEC-J2 cell migration was increased by 42% after SC addition, as opposed to non-treated cells (P ≤ 0.05). BC and SC treatments significantly reduced ETEC-mediated increases in IL-8 and CCL20 expression (P ≤ 0.05). BC treatment also significantly reduced IPEC-J2 cell monolayer permeability induction after ETEC infection. These results show that BC and SC fractions improve intestinal epithelial cell integrity and decrease ETEC-mediated inflammatory responses. Therefore, BC should be considered as a potential alternative to antibiotics.