title: Short-term glutamine supplementation decreases lung inflammation and the receptor for advanced glycation end-products expression in direct acute lung injury in mice.
abstract: BACKGROUND
  Glutamine (GLN) has been reported to improve clinical and experimental sepsis outcomes. However, the mechanisms underlying the actions of GLN remain unclear, and may depend upon the route of GLN administration and the model of acute lung injury (ALI) used. The aim of this study was to investigate whether short-term GLN supplementation had an ameliorative effect on the inflammation induced by direct acid and lipopolysaccharide (LPS) challenge in mice.
  
  
  METHODS
  Female BALB/c mice were divided into two groups, a control group and a GLN group (4.17% GLN supplementation). After a 10-day feeding period, ALI was induced by intratracheal administration of hydrochloric acid (pH 1.0; 2 mL/kg of body weight [BW]) and LPS (5 mg/kg BW). Mice were sacrificed 3 h after ALI challenge. In this early phase of ALI, serum, lungs, and bronchoalveolar lavage fluid (BALF) from the mice were collected for further analysis.
  
  
  RESULTS
  The results of this study showed that ALI-challenged mice had a significant increase in myeloperoxidase activity and expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α in the lung compared with unchallenged mice. Compared with the control group, GLN pretreatment in ALI-challenged mice reduced the levels of receptor for advanced glycation end-products (RAGE) and IL-1β production in BALF, with a corresponding decrease in their mRNA expression. The GLN group also had markedly lower in mRNA expression of cyclooxygenase-2 and NADPH oxidase-1.
  
  
  CONCLUSIONS
  These results suggest that the benefit of dietary GLN may be partly contributed to an inhibitory effect on RAGE expression and pro-inflammatory cytokines production at an early stage in direct acid and LPS-induced ALI in mice.
authors.forename: Yin-Ching
authors.initials: YC
authors.lastname: Chuang
authors.forename: Huey-Mei
authors.initials: HM
authors.lastname: Shaw
authors.forename: Chi-Chung
authors.initials: CC
authors.lastname: Chen
authors.forename: He-Jia
authors.initials: HJ
authors.lastname: Pan
authors.forename: Wei-Chih
authors.initials: WC
authors.lastname: Lai
authors.affiliation: Department of Health and Nutrition, Chia-Nan University of Pharmacy and Science, Tainan, Taiwan. cherry85@mail.chna.edu.tw.
authors.forename: Hui-Ling
authors.initials: HL
authors.lastname: Huang
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid; D051546:Cyclooxygenase 2 / Q000235:genetics; D019587:Dietary Supplements; D004789:Enzyme Activation / Q000187:drug effects; D005260:Female; D005973:Glutamine / Q000008:administration & dosage*; D006851:Hydrochloric Acid; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D008070:Lipopolysaccharides; D051379:Mice; D008807:Mice, Inbred BALB C; D009247:NADH, NADPH Oxidoreductases / Q000235:genetics; D000074624:NADPH Oxidase 1; D009195:Peroxidase / Q000378:metabolism; D011014:Pneumonia / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism*; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; D005973:Glutamine; D009195:Peroxidase; D051546:Cyclooxygenase 2; D009247:NADH, NADPH Oxidoreductases; D000074624:NADPH Oxidase 1; D006851:Hydrochloric Acid