Regulatory Effect Of Glutamic Acid Or Glycine On Intestinal Mucosal Immune Barrier Injury In Piglets After Lipopolysaccharide Challenge

The experiments were conducted to investigate the effects of glutamic acid (Glu) or glycine (Gly) supplementation on intestinal mucosal immune barrier function of weanling piglets after lipopolysaccharide (LPS) challenge and its mechanisms.1. Experiment 1 was conducted to explore the mechanism(s) by which Glu exerted its protective role on intestinal damage via modulation of stress signals. Twenty four pigs (average body weight 7.02±0.21 kg) were allotted to four treatments including:(1) control group (basal diet); (2) LPS group (basal diet+LPS); (3) 1.0% Glu group (basal diet+1.0% Glu+LPS); (4) 2.0% Glu group (basal diet+2.0% Glu+LPS). On d 28, the piglets in the LPS group,1.0% Glu group and 2.0% Glu group were injected intraperitoneally with 100 μg/kg BW LPS, and the piglets in the control group were injected with the same dose of physiological saline. The pigs were slaughtered at 4 h following saline or LPS injection to collect intestinal samples for analysis. The results showed that:1) 1.0% or 2.0% Glu significantly alleviated the increase of the number of neutrophilic granulocyte in jejunum and mastocyte in ileum and colon caused by LPS (P<0.05); 1.0% Glu tended to alleviate the increase of the number of neutrophilic granulocyte in jejunum and mastocyte and intraepithelial lymphocytes in ileum (P<0.10); 1.0% or 2.0% Glu increased the density of intraepithelial lymphocytes in jejunum, neutrophilic granulocyte in ileum and pancreatic polypeptide cells in intestinal mucosa (P<0.05).2) 1% or 2% Glu reduced the mRNA expression of corticotrophin releasing jejunal hormone (CRH) (P<0.05), glucocorticoid receptor (GR) (P<0.05) and CRHR1 (P<0.001), and tended to decrease the mRNA expression of CRHR1 in ileum and colon (P<0.10).2% Glu had a tendency to enhance the mRNA expression of GR in colon(P<0.10). These results indicate that Glu supplementation alleviates the damage in intestinal mucosal immune barrier induced by LPS, which may closely related with its inhibition of activation of intestinal stress signaling pathway.2. Experiment 2 was conducted to explore the mechanism(s) by which Gly exerted its protective role on intestinal damage via modulation of stress signaling. Twenty four pigs (average body weight 7.17±0.17 kg) were allotted to four treatments including:(1) control group (basal diet); (2) LPS group (basal diet+LPS); (3) 1.0% Gly group (basal diet+1.0% Gly+LPS); (4) 2.0% Gly group (basal diet+2.0% Gly+LPS). On d 28, the piglets in the LPS group,1.0% Gly group and 2.0% Gly group were injected intraperitoneally with 100 μg/kg BW LPS, and the piglets in the control group were injected with the same dose of physiological saline. The pigs were slaughtered at 4 h following saline or LPS injection to collect intestinal samples for analysis. The results showed that:1) 1.0% or 2.0% Gly significantly alleviated the increase of the number of jejunal and ileal neutrophils, and the increase of the number of colon mast cells caused by LPS (P<0.05); 1.0% or 2.0% Gly tended to increase the number of goblet cells in ileum and epithelium lymphocytes in colon (P<0.10); 1.0% and 2.0% Gly significantly increased the density of intestinal mucosa PP junction cell (P<0.001); 2.0% Gly significantly increased the cells of ileal lamina propria.2) 1.0% or 2.0% Gly reduced the mRNA expression of jejunum CRHR1 and GR (P<0.05), and had a tendency to decrease the mRNA expression of ileal and colonal CRHR1 (P<0.10). These results indicate that Gly alleviates the damage in intestinal mucosal immune barrier induced by LPS, which may closely related with its inhibition of activation of intestinal stress signaling pathway.