Effects of Biotite V supplementation on growth performance and the immunological responses of weaned pigs after an Escherichia coli lipopolysaccharide challenge

Abstract

This study evaluated the effect of an aluminosilicate mineral additive-Biotite V (BV) on growth performance, the immunological and adrenal responses in weaned pigs after Escherichia coli lipopolysaccharide (LPS) challenge. Thirty-two crossbred weaned pigs were used in this 2×2 factorial experiment, with dietary treatment (basal diet with or without 0.45% BV supplementation) and LPS challenge (challenged or not challenged) as two main factors. On day 14 and 21, pigs were injected intraperitoneally with either 100μg/kg body weight of LPS or an equivalent amount of sterile saline. Blood samples were collected 3h after the first challenge followed by total and differential leukocyte counts and analysis of plasma tumor necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), cortisol, insulin, and biochemical parameters. Body weight and feed intake were measured weekly throughout the 4-week experiment. The results showed that both LPS challenges reduced average daily gain (ADG) (P<0.05) and increased feed/gain (P<0.001), and BV decreased feed/gain (P<0.05) of immunology challenged pigs. The LPS challenge×diet interactions were observed for ADG (P<0.05) and feed/gain (P<0.05) during both challenge. LPS challenge reduced the number of white blood cells, lymphocytes, monocytes, and neutrophils (P<0.05). LPS challenge×diet interaction was observed for plasma TNF-α (P<0.05) concentration, showing decreased plasma TNF-α response to LPS challenged in pigs receiving BV. But no LPS challenge × diet interaction was observed for plasma cortisol or PGE2. There was a diet effect for plasma insulin (P<0.05) and glucose (P<0.05), showing increased plasma insulin and decreased glucose with BV supplementation, but no LPS challenge×diet interaction was observed. We conclude that BV improved the weight gain and feed efficiency of weaned pigs during an immunological challenge by suppressing the proinflammatory cytokine release.