Weaning diet supplemented with health-promoting feed additives influences microbiota and immune response in piglets challenged with Salmonella

The aim of this study was to evaluate the potential of micronutrients and feed additives to modulate intestinal microbiota and systemic and mucosal immune responses in weaned pigs infected with Salmonella. At weaning, 32 litters of 12 piglets each were allocated to four dietary treatments: 1) control diet (CTRL), 2) CTRL supplemented with chlortetracycline (ATB), 3) CTRL supplemented with a cocktail of feed additives (CKTL); and 4) CKTL diet containing bovine colostrum in replacement of spray-dry animal plasma (CKTL+COL). The CKTL supplement included cranberry extract, encapsulated carvacrol and yeast-derived products and an enriched selenium and vitamin premix. Three weeks after weaning, four pigs per litter were orally inoculated with Salmonella Typhimurium DT104. Half of them were euthanized 3 days post-infection (dpi) and the other half, 7 dpi. The expression of IL6, TNF, IL8, monocyte chemoattractant protein 1 (MCP1), IFNG, cyclooxygenase 2 (COX2), glutathione peroxidase 2 (GPX2) and β-defensin 2 (DEFB2) showed a peaked response at 3 dpi (P < 0.05). Results also revealed that DEFB2 expression was higher at 3 dpi in CTRL and CKTL groups than in ATB (P = 0.01 and 0.06, respectively) while GPX2 gene was markedly increased at 3 and 7 dpi in pigs fed CKTL or CKTL+COL diet compared to CTRL pigs (P < 0.05). In piglets fed CKTL or CKTL+COL diet, intestinal changes in microbial communities were less pronounced after exposure to Salmonella compared to CTRL and progressed faster toward the status before Salmonella challenge (AMOVA P < 0.01). Furthermore, the relative abundance of several families was either up- or down-regulated in pigs fed CKTL or CKTL+COL diet after Salmonella challenge. In conclusion, weaning diet enriched with bovine colostrum, vitamins and mixture of feed additives mitigated the influence of Salmonella infection on intestinal microbial populations and modulate systemic and intestinal immune defences.