title: Intestinal dendritic cells change in number in fulminant hepatic failure.
abstract: OBJECTIVE
  To investigate the change in intestinal dendritic cell (DC) number in fulminant hepatic failure (FHF).
  
  
  METHODS
  An animal model of FHF was created. Intestinal CD11b/c was detected by immunohistochemistry and Western blot. Quantitative real-time polymerase chain reaction (PCR) was used to detect intestinal integrin-α mRNA expression. Intestinal CD83, CD86, CD74, CD3 and AKT were detected by immunohistochemistry, Western blot and PCR. Phosphorylated-AKT (p-AKT) was detected by immunohistochemistry and Western blot.
  
  
  RESULTS
  In the FHF group [D-galactosamine (D-Galn) + lipopolysaccharide (LPS) group], the mice began to die after 6 h; conversely, in the D-Galn and LPS groups, the activity of mice was poor, but there were no deaths. Immunohistochemistry results showed that in FHF, the expression of CD11b/c (7988400 ± 385941 vs 1102400 ± 132273, P < 0.05), CD83 (13875000 ± 467493 vs 9257600 ± 400364, P < 0.05), CD86 (7988400 ± 385941 vs 1102400 ± 13227, P < 0.05) and CD74 (11056000 ± 431427 vs 4633400 ± 267903, P < 0.05) was significantly increased compared with the normal saline (NS) group. Compared with the NS group, the protein expression of CD11b/c (5.4817 ± 0.77 vs 1.4073 ± 0.37, P < 0.05) and CD86 (4.2673 ± 0.69 vs 1.1379 ± 0.42, P < 0.05) was significantly increased. Itg-α (1.1224 ± 0.3 vs 0.4907 ± 0.19, P < 0.05), CD83 (3.6986 ± 0.40 vs 1.0762 ± 0.22, P < 0.05) and CD86 (1.5801 ± 0.32 vs 0.8846 ± 0.10, P < 0.05) mRNA expression was increased significantly in the FHF group. At the protein level, expression of CD74 in the FHF group (2.3513 ± 0.52) was significantly increased compared with the NS group (1.1298 ± 0.33), whereas in the LPS group (2.3891 ± 0.47), the level of CD74 was the highest (P < 0.05). At the gene level, the relative expression of CD74 mRNA in the FHF group (1.5383 ± 0.26) was also significantly increased in comparison to the NS group (0.7648 ± 0.22; P < 0.05). CD3 expression was the highest in the FHF group (P < 0.05). In the FHF, LPS and D-Galn groups, the expression of AKT at the protein and mRNA levels was elevated compared with the NS group, but there was no statistical significance (P > 0.05). The p-AKT protein expression in the FHF (1.54 ± 0.06), LPS (1.56 ± 0.05) and D-Galn (1.29 ± 0.03) groups was higher than that in the NS group (1.07 ± 0.03) (P < 0.05).
  
  
  CONCLUSIONS
  In FHF, a large number of DCs mature, express CD86, and activate MHC class II molecular pathways to induce a T cell response, and the AKT pathway is activated.
authors.affiliation: Xu Cao, Mei Liu, Peng Wang, Dong-Yan Liu, Research Center, Shengjing Hospital of China Medical University and Key Laboratory of Congenital Malformation Research, Ministry of Health, Shenyang 110004, Liaoning Province, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Cao
authors.affiliation: Xu Cao, Mei Liu, Peng Wang, Dong-Yan Liu, Research Center, Shengjing Hospital of China Medical University and Key Laboratory of Congenital Malformation Research, Ministry of Health, Shenyang 110004, Liaoning Province, China.
authors.forename: Mei
authors.initials: M
authors.lastname: Liu
authors.affiliation: Xu Cao, Mei Liu, Peng Wang, Dong-Yan Liu, Research Center, Shengjing Hospital of China Medical University and Key Laboratory of Congenital Malformation Research, Ministry of Health, Shenyang 110004, Liaoning Province, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Wang
authors.affiliation: Xu Cao, Mei Liu, Peng Wang, Dong-Yan Liu, Research Center, Shengjing Hospital of China Medical University and Key Laboratory of Congenital Malformation Research, Ministry of Health, Shenyang 110004, Liaoning Province, China.
authors.forename: Dong-Yan
authors.initials: DY
authors.lastname: Liu
mesh_terms: D000818:Animals; D000944:Antigens, Differentiation, B-Lymphocyte / Q000378:metabolism; D051940:B7-2 Antigen / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D039481:CD11b Antigen / Q000378:metabolism; D039521:CD11c Antigen / Q000378:metabolism; D017252:CD3 Complex / Q000378:metabolism; D002450:Cell Communication; D002452:Cell Count; D003713:Dendritic Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D000949:Histocompatibility Antigens Class II / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000276:immunology / Q000473:pathology*; D017114:Liver Failure, Acute / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D008213:Lymphocyte Activation; D008807:Mice, Inbred BALB C; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
chemical_list: D000944:Antigens, Differentiation, B-Lymphocyte; D051940:B7-2 Antigen; D015415:Biomarkers; D039481:CD11b Antigen; D039521:CD11c Antigen; D017252:CD3 Complex; C497965:Cd86 protein, mouse; D000949:Histocompatibility Antigens Class II; C045084:invariant chain; D051057:Proto-Oncogene Proteins c-akt
keywords: AKT/Phosphorylated-AKT; CD3; Fulminant hepatic failure; Intestinal dendritic cells; MHC II