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

The experiments were conducted to investigate the effects of asparticacid (ASP) or asparagine (ASN) supplementation on intestinal mucosalimmune barrier function of weanling piglets after lipopolysaccharide(LPS) challenge and its mechanisms.1. Experiment1was conducted to explore the mechanism(s) bywhich ASP exerted its protective role on intestinal damage via modulationof stress signals. Twenty four pigs (average body weight7.37±0.04kg)were allotted to four treatments including:(1) control group;(2) LPSgroup;(3) LPS+0.5%ASP group;(4) LPS+1.0%ASP group. The pigs wereslaughtered after24h LPS challenge to collect intestinal samples foranalysis. The results showed that:1)0.5%or1.0%ASP alleviated thedecrease of jejunal villus height and villus height/crypt depth and theincrease of crypt depth induced by LPS, and increased ileal villus heightand villus height/crypt depth and0.5%ASP increased colonic crypt depth(P<0.05).2)0.5%or1.0%ASP alleviated the increase of the numbers ofjejunal intraepithelial lymphocytes, neutrophils, mast cells and ileal mastcells and colonic goblet cells(P<0.05).0.5%or1.0%ASP reduced thenumbers of ileal intraepithelial lymphocytes and goblet cells (P<0.05).3)0.5%or1.0%ASP reduced mRNA expression of corticotropin releasinghormone (CRH) in ileum, glucocorticoid receptor(GR) in jejunum andileum, and tryptase in jejunum.0.5%or1.0%ASP increased mRNAexpression of corticotropin releasing hormone receptor one (CRHR1) incolon (P<0.05) and ileum (P<0.10). These results indicate that ASPalleviates the damage in intestinal mucosal immune barrier induced byLPS, which may closely related with its inhibition of activation ofintestinal stress signaling pathway. 2. Experiment2was conducted to explore the mechanism(s) bywhich ASN exerted its protective role on intestinal damage viamodulation of stress signals. Twenty four pigs (average body weight8.07±0.75kg) were allotted to four treatments including:(1) controlgroup;(2) LPS group;(3) LPS+0.5%ASN group;(4) LPS+1.0%ASNgroup. The pigs were slaughtered after24h LPS challenge to collectintestinal samples for analysis. The results showed that:1)0.5%or1.0%ASN alleviated the decrease of jejunal villus height and villusheight/crypt depth induced by LPS, and increased ileal villus height andvillus height/crypt depth, and decreased jejunal crypt depth (P<0.05).2)0.5%or1.0%ASN alleviated the increase of the number of jejunalintraepithelial lymphocytes, neutrophils, mast cells and colonic gobletcells induced by LPS (P<0.05).0.5%ASN had a tendency to alleviate theincrease of the number of ileal mast cells (P<0.10).0.5%or1.0%ASN hada tendency to reduce the numbers of colonic intraepithelial lymphocytesand neutrophils (P<0.10).3)0.5%or1.0%ASN alleviated the increase ofthe number of ilea Peyer’s patches (PP) induced by LPS (P<0.05).0.5%ASNreduced cell density of PP in ileum.4)1.0%ASN alleviated the increaseof cell density of lamina propria in jejunum induced by LPS (P<0.05).1.0%ASN reduced cell density of lamina propria in ileum (P<0.05).5)0.5%or1.0%ASN reduced mRNA expression of CRH in ileum, GR injejunum and ileum, tryptase in jejunum (P<0.05).1.0%ASN increasedmRNA expression of CRHR1in ileum and colon (P<0.05). These resultsindicate that ASN alleviate the damage in intestinal mucosal immunebarrier induced by LPS, which may closely related with its inhibition ofactivation of intestinal stress signaling pathway.