Abstract | GOALS: This study attempts to determine expressions of intrahepatic proinflammatory and anti-inflammatory cytokines and their secreting immunocytes to evaluate their roles in the pathogenesis of acute-on-chronic liver failure (ACLF) in chronically hepatitis B virus (HBV)-infected patients. BACKGROUND: ACLF generally affects patients with established, compensated chronic liver diseases who develop an acute deterioration in liver function. In China, HBV-associated ACLF patients account for more than 80% of ACLF patients owing to a high prevalence of chronic HBV infection. Clinical observation showed that the deterioration of this disease may correlate with host immune responses, but related underlying mechanism remains largely unknown. STUDY: RESULTS: Intrahepatic proinflammatory IFN-gamma and TNF-alpha expressions were markedly up-regulated in ACLF compared with CHB and NC. However, similar anti-inflammatory IL-10 expressions were observed in ACLF and CHB. IFN-gamma overexpression correlated significantly with increased CD4 and CD8 T-cell accumulation. TNF-alpha up-regulation also correlated significantly with increased KCs. CONCLUSIONS: The imbalanced expression of proinflammatory and anti-inflammatory cytokines and increased accumulation of CD4, CD8 T cells, and KCs may contribute to immunopathogenesis in HBV-infected ACLF.
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Authors | Zhengsheng Zou, Baosen Li, Dongping Xu, Zheng Zhang, Jing-Min Zhao, Guangde Zhou, Yanling Sun, Lei Huang, Junliang Fu, Yongping Yang, Lei Jin, Wei Zhang, Jun Zhao, Ying Sun, Shaojie Xin, Fu-Sheng Wang |
Journal | Journal of clinical gastroenterology
(J Clin Gastroenterol)
Vol. 43
Issue 2
Pg. 182-90
(Feb 2009)
ISSN: 1539-2031 [Electronic] United States |
PMID | 18633332
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Cytokines
- Tumor Necrosis Factor-alpha
- Interleukin-10
- Interferon-gamma
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Topics |
- Adult
- Aged
- CD4-Positive T-Lymphocytes
(immunology)
- CD8-Positive T-Lymphocytes
(immunology)
- Cytokines
(metabolism)
- Female
- Hepatitis B virus
(immunology, pathogenicity)
- Hepatitis B, Chronic
(immunology, physiopathology, virology)
- Humans
- Immunohistochemistry
- Interferon-gamma
(metabolism)
- Interleukin-10
(metabolism)
- Kupffer Cells
(immunology)
- Liver
(cytology, immunology)
- Liver Cirrhosis
(immunology, physiopathology, virology)
- Liver Failure, Acute
(immunology, physiopathology, virology)
- Lymphocyte Activation
- Male
- Middle Aged
- Tumor Necrosis Factor-alpha
(metabolism)
- Up-Regulation
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