Basic Study
Copyright ©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 28, 2015; 21(16): 4883-4893
Published online Apr 28, 2015. doi: 10.3748/wjg.v21.i16.4883
Intestinal dendritic cells change in number in fulminant hepatic failure
Xu Cao, Mei Liu, Peng Wang, Dong-Yan Liu
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
Author contributions: Cao X performed the research, analyzed the data and wrote the paper; Liu M analyzed the data and revised the manuscript; Wang P analyzed the data; Liu DY designed the research, performed the research, wrote and revised the manuscript.
Supported by National Natural Science Foundation of China, No. 30871158 and No. 81170604; and Outstanding Scientific Fund of Shengjing Hospital.
Conflict-of-interest: The authors declare that there is no conflict of interest regarding the publication of this paper.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dong-Yan Liu, Professor, Research Center, Shengjing Hospital of China Medical University and Key Laboratory of Congenital Malformation Research, Ministry of Health, No. 36 Sanhao Street, Heping District, Shenyang 110004, Liaoning Province, China. dongyan.liu@aliyun.com
Telephone: +86-24-96615-13427 Fax: +86-24-23929903
Received: September 15, 2014
Peer-review started: September 19, 2014
First decision: October 29, 2014
Revised: December 17, 2014
Accepted: January 16, 2015
Article in press: January 16, 2015
Published online: April 28, 2015
Processing time: 224 Days and 4.5 Hours
Abstract

AIM: 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).

CONCLUSION: 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.

Keywords: Fulminant hepatic failure; Intestinal dendritic cells; MHC II; CD3; AKT/Phosphorylated-AKT

Core tip: In this study, we showed that the expression of CD11b/c, CD83, CD86, CD74 and CD3 in the fulminant hepatic failure (FHF) group [D-galactosamine (D-Galn) + lipopolysaccharide (LPS) group] was significantly higher compared with the normal saline (NS) group. Additionally, the phosphorylated-AKT protein expression in the FHF, LPS and D-Galn groups was higher than that in the NS group. This result showed that a large number of dendritic cells mature, express CD86, and activate MHC class II molecular pathways to induce a T cell response in FHF. In addition, the AKT pathway in FHF was activated.