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Mediators of Inflammation
Volume 2017, Article ID 1390458, 10 pages
https://doi.org/10.1155/2017/1390458
Research Article

Deregulation of Regulatory T Cells in Acute-on-Chronic Liver Failure: A Rat Model

1Department of Infectious Diseases, Jinhua Municipal Central Hospital, Jinhua, Zhejiang, China
2Department of Infectious Diseases, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou Key Laboratory of Hepatology, Hepatology Institute of Wenzhou Medical University, Wenzhou, Zhejiang, China
3Department of Infectious Diseases, Ruian City People’s Hospital, The Third Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China

Correspondence should be addressed to Mingqin Lu; moc.361@6090qml

Received 14 April 2016; Revised 20 October 2016; Accepted 26 October 2016; Published 15 January 2017

Academic Editor: Alex Kleinjan

Copyright © 2017 Shunlan Ni et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Aims. Acute-on-chronic liver failure (ACLF) and acute liver failure (ALF) are similar in many respects during their acute exacerbation; however, ACLF generally has a poorer prognosis. We aimed to investigate the role and dynamic changes of regulatory T cell (Treg) and T helper 17 (Th17) cell proportions during ACLF progress. Methods. All rats were classified into two groups randomly: ACLF group and ALF group (control group). The rat model of ACLF was preestablished by intraperitoneal injection of carbon tetrachloride for 2 months. Then acute liver injury was induced by combined D-galactosamine and lipopolysaccharide. Six time points were examined before or after acute induction. Liver samples were performed with hematoxylin-eosin and Masson staining; circulatory Treg and Th17 cell frequencies were determined using flow cytometry assays; serum levels of alanine aminotransferase, aspartate aminotransferase, interleukin-10 (IL-10), and interferon-γ (IFN-γ) were examined. Results. In group ACLF, both Th17 cell proportion and IFN-γ level presented upgrade firstly and then descend latter tendency; the trends of Treg cell proportion and IL-10 level were observed to gradually decrease and became stable. Conclusion. The Treg cells played an important role in the immunologic mechanism during the process of ACLF. And the function of Treg cells in ACLF was defective.