title: Glutamine attenuates lipopolysaccharide-induced acute lung injury.
abstract: OBJECTIVE
  It has been reported that glutamine (GLN) can attenuate acute lung injury after sepsis. GLN is also thought to be a precursor of glutathione (GSH) synthesis. Using the GSH synthesis blocker, L-buthionine-(S,R)-sulfoximine (BSO), we investigated the role of GSH synthesis in the protective effect of GLN on acute lung injury.
  
  
  METHODS
  In this study, we used an acute lung injury model induced by intratracheal injection of lipopolysaccharide (1 mg mL(-1) kg(-1)). GLN (0.75 g/kg, intravenous) and BSO (2 mmol/kg, intraperitoneal) were administrated simultaneously. At 2 and 18 h after the injections, the rats were sacrificed by right ventricular puncture and bronchoalveolar lavage was done. The lower right lung was excised for histologic examination. Total protein concentration and total cell and neutrophil counts in the bronchoalveolar lavage fluid were determined. CD11b expression in the blood was determined by flow cytometry. We also analyzed myeloperoxidase activity, and GSH and interleukin-8 levels in lung tissues.
  
  
  RESULTS
  GLN supplementation reduced the total protein concentration and total cell and neutrophils counts in bronchoalveolar lavage fluid after lipopolysaccharide challenge. GLN enhanced GSH synthesis and attenuated interleukin-8 release and myeloperoxidase activity in lung tissues. GLN also decreased CD11b expression in blood neutrophils and prevented lung histologic changes. BSO abolished the effects of GLN and attenuated its protection on acute lung injury.
  
  
  CONCLUSIONS
  These results indicate that GLN could prevent neutrophil recruitment and infiltration, protect the alveolar barrier, and attenuate inflammatory injury during sepsis. This effect may be related to enhanced GSH synthesis.
authors.affiliation: Research Institute of General Surgery, Department of General Surgery, Jinling Hospital, Medical School, Nanjing University, Nanjing, Jiangsu Province, People's Republic of China.
authors.forename: Feng
authors.initials: F
authors.lastname: Zhang
authors.forename: Xinying
authors.initials: X
authors.lastname: Wang
authors.forename: Liya
authors.initials: L
authors.lastname: Pan
authors.forename: Weiya
authors.initials: W
authors.lastname: Wang
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D055371:Acute Lung Injury / Q000139:chemically induced / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D000818:Animals; D018893:Bronchoalveolar Lavage; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D019328:Buthionine Sulfoximine / Q000494:pharmacology; D039481:CD11b Antigen / Q000378:metabolism; D018821:CD18 Antigens / Q000378:metabolism; D004195:Disease Models, Animal; D005973:Glutamine / Q000378:metabolism* / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism* / Q000502:physiology; D007249:Inflammation; D016209:Interleukin-8 / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D008168:Lung / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D008297:Male; D009504:Neutrophils / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D039481:CD11b Antigen; D018821:CD18 Antigens; D016209:Interleukin-8; D008070:Lipopolysaccharides; D005973:Glutamine; D019328:Buthionine Sulfoximine; D009195:Peroxidase; D005978:Glutathione