title: [Comparation of inflammation between wild mice and severe combined immunodeficiency mice with endotoxemia induced by lipopolysaccharide].
abstract: OBJECTIVE
  To compare the inflammation between wild BALB/c mice and mice with severe combined immunodeficiency (SCID) with endotoxemia induced by lipopolysaccharide (LPS).
  
  
  METHODS
  Endotoxemia models of wild and SCID mice were established by injecting LPS intraperitoneally. Serum was taken before and 3 h, 6 h, 12 h after injecting LPS, liver and lung were taken 12 h after injecting LPS. Alanine transarninase (ALT), aspartate aminotransferase (AST) and blood urea nitrogen (BUN) levels were measured by automatic biochemical analyzer. Liver and lung inflammation injury were observed by H.E staining. TNF-α, IFN-γ, IL-6 and MCP-1 levels in serum were detected by Cytometric Bead Array (CBA).
  
  
  RESULTS
  (1) All of SCID mice (8/8) were dead at 12-24 h after injecting LPS, and only one BALB/c mouse (1/8) was dead. (2) ALT and AST levels of SCID mice 12 h after injecting LPS were higer than those of BALB/c mice(P<0.05), but there was no difference of BUN levels between them. (3) The blind liver and lung pathology scores of SCID mice were higher than those of BALB/c mice (P<0.05). (4) TNF-α, IFN-γ, IL-6 and MCP-1 levels in serum at 3 h, 6 h, 12 h after injecting LPS increased significantly, and the cytokine levels of SCID mice were higher than those of BALB/c mice(P<0.05).
  
  
  CONCLUSIONS
  SCID mice don't only excessively secrete inflammatory cytokines after injecting LPS, but also lead to more severe endotoxemia and inflammation injury of organs, which are the important cause of mouse death. The above results also show that the adjustment deficiency of adaptive immunoresponse, abnormal augmentation of innate immunoresponse may be an important cause of severe SIRS of endangering life.
authors.affiliation: Ministry of Education Key Laboratory of Child Development and Disorders, Children's Hospital, Chongqing Medical University, Chongqing 400014, China. luochong@yahoo.cn
authors.forename: Chong
authors.initials: C
authors.lastname: Luo
authors.forename: Xi-qiang
authors.initials: XQ
authors.lastname: Yang
authors.forename: Xin
authors.initials: X
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Liu
authors.forename: Li-jiang
authors.initials: LJ
authors.lastname: Wang
mesh_terms: D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D001806:Blood Urea Nitrogen; D018932:Chemokine CCL2 / Q000097:blood; D019446:Endotoxemia / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D007249:Inflammation / Q000139:chemically induced / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D007371:Interferon-gamma / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides; D008099:Liver / Q000473:pathology; D008168:Lung / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase