Effects of Lactobacillus acidophilus dietary supplementation on the performance, intestinal barrier function, rectal microflora and serum immune function in weaned piglets challenged with Escherichia coli lipopolysaccharide

This study was conducted with a lipopolysaccharide (LPS)-challenged piglet model to determine the effects of diets containing Lactobacillus acidophilus on the performance, intestinal barrier function, rectal microflora and serum immune function. A total of 150 piglets (initial body weight (BW) 7.53 +/- A 0.21 kg) were allotted to one of the following diets, including a basal diet, a basal diet supplemented with 250 mg/kg Flavomycin, or basal diet plus 0.05, 0.1 or 0.2 % L. acidophilus. On day 28 of the trial, the pigs were given an intraperitoneal injection of LPS (200 mu g/kg body weight) followed by blood collection 3 h later. Diets with either antibiotics, 0.1 or 0.2 % Lactobacillus increased (P < 0.05) the final BW and decreased (P < 0.05) feed gain ratio (F/G) compared with the control group. Pigs fed diets containing antibiotic or Lactobacillus had greater average daily gain (ADG) (P < 0.05) than pigs fed the control diet. The rectal content Lactobacillus counts for pigs fed diet containing Lactobacillus were significant higher (P < 0.01) than those fed antibiotic or control diet. Feeding the Lactobacillus diets decreased the Escherichia coli counts of rectal content (P < 0.01). Pigs fed diets containing 0.1 or 0.2 % Lactobacillus decreased serum DAO activity (P < 0.05) compared with pigs fed the control diet. Serum IL-10 concentration was enhanced in pigs fed the diet with Lactobacillus compared to pigs fed the control diet and antibiotic diet. Feeding a diet with Lactobacillus reduced (P < 0.05) IFN-gamma concentration compared to the control diet. Inclusion of Lactobacillus in diets fed to pigs reduced TNF-alpha concentration compared with pigs fed no Lactobacillus (P < 0.05). These results indicate that feeding with L. acidophilus improved growth performance and protected against LPS-induced inflammatory status.