Yeast hydrolysate attenuates lipopolysaccharide-induced inflammatory responses and intestinal barrier damage in weaned piglet

Abstract

Background Yeast hydrolysate (YH) has attracted much attention as a nutritional additive, and it is generally considered to be non-toxic, effective and safe. However, there is still inconclusive on the effects of dietary YH supplementation on immunity function and intestinal barrier of piglets. This study was conducted to investigate the effects of YH supplementation on inflammatory responses and intestinal barrier in piglets challenged with lipopolysaccharide. Methods Twenty-four piglets (with an average body weight of 7.42 ± 0.34 kg) weaned at 21 days of age were randomly fed a diet containing 0 or 0.5% yeast hydrolysate for 21 days. On the 22nd day, half of piglets were intraperitoneally injected with lipopolysaccharide at 150 µg/kg BW, and the other half were injected with an equal volume of sterile normal saline. Four hours later, blood samples of each piglet were collected and then piglets were slaughtered. Results LPS injection increased serum levels of adrenocorticotropic hormone (ACTH), cortisol, haptoglobin (HP), serum amyloid A protein (SAA), tumor necrosis factor-α (TNF-α), and diamine oxidase (DAO) (P < 0.05), decreased the jejunal villus height, the protein and mRNA abundances of zonula occludens-1 (ZO-1) and occludin (OCLN) (P < 0.05), enhanced the protein and mRNA abundances of TNF-α, interleukin-1β (IL-1β), toll-like receptors 4 (TLR4) and phosphor-Nuclear factor-κB-p65 (p-NFκB-p65) (P < 0.01). Dietary YH supplementation attenuated the impaired effects of ACTH, cortisol, HP, IL-1β, and DAO in serum (P < 0.05). Furthermore, YH supplementation up-regulated the villus height, protein and mRNA abundances of ZO-1 and OCC (P < 0.05), downregulated TNF-α, IL-1β, TLR4 and p-NFκB-p65 mRNA expressions and the corresponding protein abundances in the jejunum in LPS-challenged pigs (P < 0.01). Conclusion YH could alleviate inflammatory response and intestinal barrier injury in weaned piglets challenged with LPS, which was associated with inhibited the TLR4/NF-κB signaling pathway.