title: Decreased IgA+ plasma cells and IgA expression in acute liver necrosis mice.
abstract: OBJECTIVE
  To investigate the number of intestinal immunoglobulin A (IgA+) plasma cells and expression of intestinal IgA in mice with acute liver necrosis.
  
  
  METHODS
  A model of acute liver necrosis was established by intraperitoneal injection of galactosamine (GalN) and lipopolysaccharide (LPS). Sixty mice were randomly divided into one of 4 equal groups: normal control, acute liver necrosis, LPS, or GalN. Hematoxylin and eosin staining, immunohistochemistry, and an enzyme-linked immunosorbent assay were employed to assess liver and intestinal injury, count intestinal IgA+ plasma cells, and measure the expression level of IgA and interferon gamma (IFN-gamma) in the small intestinal mucosa of mice.
  
  
  RESULTS
  Injured intestinal mucosa was observed in the acute liver necrosis group but not in the normal, LPS or GalN groups. Compared with the normal group, intestinal IgA+ plasma cells were slightly decreased in the LPS and GalN groups [429 +/- 20 per high power field (HPF), 406 +/- 18/HPF, respectively], whereas they were markedly decreased in the acute liver necrosis group (282 +/- 17/HPF vs 495 +/- 26/HPF in normal group, P < 0.05). The expression of intestinal IgA was also slightly decreased in LPS and GalN groups, but was markedly reduced in the acute liver necrosis group as determined by enzyme-linked immunosorbent assay (P < 0.05). In contrast, the level of IFN-gamma was slightly increased in LPS, GalN and acute liver necrosis groups, but with no statistical significance (P > 0.05).
  
  
  CONCLUSIONS
  Intestinal IgA+ plasma cells and IgA expression levels indicating that mucosal immune barrier dysfunction, does exist in acute liver necrosis.
authors.affiliation: Department of Infectious Diseases, The First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning Province, China.
authors.forename: Jin-Long
authors.initials: JL
authors.lastname: Fu
authors.forename: Zhao-Han
authors.initials: ZH
authors.lastname: Wang
authors.forename: Guo-Zhen
authors.initials: GZ
authors.lastname: Li
authors.forename: Yu-Rong
authors.initials: YR
authors.lastname: Wang
authors.forename: Pei
authors.initials: P
authors.lastname: Liu
mesh_terms: D000208:Acute Disease; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D015536:Down-Regulation; D004797:Enzyme-Linked Immunosorbent Assay; D005688:Galactosamine; D018928:Immunity, Mucosal; D007070:Immunoglobulin A / Q000378:metabolism*; D007371:Interferon-gamma / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology; D007421:Intestine, Small / Q000276:immunology* / Q000473:pathology; D008070:Lipopolysaccharides; D008099:Liver / Q000473:pathology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009336:Necrosis; D010950:Plasma Cells / Q000276:immunology*; D013194:Staining and Labeling
chemical_list: D007070:Immunoglobulin A; D008070:Lipopolysaccharides; D005688:Galactosamine; D007371:Interferon-gamma; D000410:Alanine Transaminase