title: Dietary arginine supplementation alleviates intestinal mucosal disruption induced by Escherichia coli lipopolysaccharide in weaned pigs.
abstract: This study evaluated whether arginine (Arg) supplementation could attenuate gut injury induced by Escherichia coli lipopolysaccharide (LPS) challenge through an anti-inflammatory role in weaned pigs. Pigs were allotted to four treatments including: (1) non-challenged control; (2) LPS-challenged control; (3) LPS+0.5 % Arg; (4) LPS+1.0 % Arg. On day 16, pigs were injected with LPS or sterile saline. At 6 h post-injection, pigs were killed for evaluation of small intestinal morphology and intestinal gene expression. Within 48 h of challenge, 0.5 % Arg alleviated the weight loss induced by LPS challenge (P = 0.025). In all three intestinal segments, 0.5 or 1.0 % Arg mitigated intestinal morphology impairment (e.g. lower villus height and higher crypt depth) induced by LPS challenge (P < 0.05), and alleviated the decrease of crypt cell proliferation and the increase of villus cell apoptosis after LPS challenge (P < 0.01). The 0.5 % Arg prevented the elevation of jejunal IL-6 mRNA abundance (P = 0.082), and jejunal (P = 0.030) and ileal (P = 0.039) TNF-alpha mRNA abundance induced by LPS challenge. The 1.0 % Arg alleviated the elevation of jejunal IL-6 mRNA abundance (P = 0.053) and jejunal TNF-alpha mRNA abundance (P = 0.003) induced by LPS challenge. The 0.5 % Arg increased PPARgamma mRNA abundance in all three intestinal segments (P < 0.10), and 1.0 % Arg increased duodenal PPARgamma mRNA abundance (P = 0.094). These results indicate that Arg supplementation has beneficial effects in alleviating gut mucosal injury induced by LPS challenge. Additionally, it is possible that the protective effects of Arg on the intestine are associated with decreasing the expression of intestinal pro-inflammatory cytokines through activating PPARgamma expression.
authors.affiliation: Hubei Key Laboratory of Animal Nutrition and Feed Science, Wuhan Polytechnic University, Wuhan 430023, China. yulanflower@126.com
authors.forename: Yulan
authors.initials: Y
authors.lastname: Liu
authors.forename: Jingjing
authors.initials: J
authors.lastname: Huang
authors.forename: Yongqing
authors.initials: Y
authors.lastname: Hou
authors.forename: Huiling
authors.initials: H
authors.lastname: Zhu
authors.forename: Shengjun
authors.initials: S
authors.lastname: Zhao
authors.forename: Binying
authors.initials: B
authors.lastname: Ding
authors.forename: Yulong
authors.initials: Y
authors.lastname: Yin
authors.forename: Ganfeng
authors.initials: G
authors.lastname: Yi
authors.forename: Junxia
authors.initials: J
authors.lastname: Shi
authors.forename: Wei
authors.initials: W
authors.lastname: Fan
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D001120:Arginine / Q000008:administration & dosage*; D015415:Biomarkers / Q000032:analysis; D019587:Dietary Supplements; D004386:Duodenum; D004926:Escherichia coli; D005260:Female; D007082:Ileum; D015850:Interleukin-6 / Q000032:analysis / Q000235:genetics; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D007421:Intestine, Small; D007583:Jejunum; D008070:Lipopolysaccharides; D008297:Male; D047495:PPAR gamma / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D013552:Swine / Q000254:growth & development* / Q000276:immunology / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000235:genetics; D014886:Weaning
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D015850:Interleukin-6; D008070:Lipopolysaccharides; D047495:PPAR gamma; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D001120:Arginine