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1.  Plasma Interleukin-10: A Likely Predictive Marker for Hepatitis B Virus-Related Acute-on-Chronic Liver Failure 
Hepatitis Monthly  2014;14(7):e19370.
Background:
The pathogenesis of HBV-related acute-on-chronic liver failure (HBV-ACLF) is mainly based on a heightened immune-inflammatory reaction; however, the intimate underlying mechanism remains unclear.
Objectives:
The aim of the study was to explore potential key immune molecular targets that could serve as early predictive markers for HBV-ACLF.
Patients and Methods:
Twenty-seven patients with acute exacerbation of chronic hepatitis B (CHB) (defined by: alanine transaminase ≥ 20 ULN, total bilirubin ≥ 5 ULN, 40% < prothrombin time activity ≤ 60%) and without cirrhosis were divided into 18 cases which did not progress to HBV-ACLF (defined by: prothrombin time activity < 40% and development within four weeks of hepatic encephalopathy and/or ascites) and nine cases that developed HBV-ACLF. Nine healthy people defined the normal control group (NC). Interleukin-1β (IL-1β), IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, TNF-α and IFN-γ protein levels were assayed by Cytometric Bead Array (CBA) in blood plasma. The ELISA method was applied to confirm IL-10 detection using the CBA method.
Results:
IL-4, IL-12p70 and IFN-γ were undetectable; IL-1β, IL-6, IL-8, IL-10 and TNF-α levels were significantly higher than in NC. Moreover, cytokines reached the highest levels in acute exacerbation of CHB, with the exception of IL-2 and IL-8. When comparing the HBV-ACLF patients prior to and at the time of ACLF diagnosis, IL-10 was the only cytokine that exhibited a significant decrease (P = 0.008). IL-10 concentrations were positively correlated to ALT levels (r = 0.711, P < 0.001).
Conclusions:
The assessment of plasma IL-10 levels in chronic hepatitis B acute exacerbation may provide an early predictive marker for progression to HBV-ACLF.
doi:10.5812/hepatmon.19370
PMCID: PMC4139694  PMID: 25147572
Chronic Hepatitis B; Severe Exacerbation; Chronic Liver Failure; Cytokines; Interleukin-10
2.  Expansion of myeloid-derived suppressor cells from peripheral blood decreases after 4-week antiviral treatment in patients with chronic hepatitis C 
Myeloid-derived suppressor cells (MDSCs) are one of the most important regulators of anti-tumor T-cell responses in cancers. This study aimed to investigate MDSCs in the peripheral blood of patients with chronic hepatitis C (CHC) before and after 4-week treatment with pegylated interferon (PEG-IFN) and ribavirin, and to evaluate their correlation with CD4+CD25high regulatory T cells (Tregs) and clinical parameters. A total of 80 patients with CHC were enrolled into this study, 37 of whom were treated with PEG-IFN and ribavirin. Compared with healthy controls (0.462% [range 0.257%-0.634%]), the proportion of MDSCs in the peripheral blood of 80 CHC patients (0.601% [range 0.333%-1.027%]) increased significantly before therapy (P=0.011). For 37 HCV patients, the proportion of circulating MDSCs (0 w: 0.597% [range 0.296%-1.021%], 4 w: 0.126% [0.066%-0.239%], P<0.01) and Tregs (0 w: 2.467±0.927%, 4 w: 2.074±0.840%, P=0.047) decreased significantly after 4-week antiviral treatment. No significant correlation was found between MDSCs and Tregs. These findings suggest that MDSCs expand in the peripheral blood of CHC patients, but decrease after 4-week antiviral treatment.
PMCID: PMC4057852  PMID: 24955173
Myeloid-derived suppressor cells; hepatitis virus C; interferon; regulatory T cells; immunosuppression
3.  HGF and Direct Mesenchymal Stem Cells Contact Synergize to Inhibit Hepatic Stellate Cells Activation through TLR4/NF-kB Pathway 
PLoS ONE  2012;7(8):e43408.
Aims
Bone marrow-derived mesenchymal stem cells (BMSCs) can reduce liver fibrosis. Apart from the paracrine mechanism by which the antifibrotic effects of BMSCs inhibit activated hepatic stellate cells (HSCs), the effects of direct interplay and juxtacrine signaling between the two cell types are poorly understood. The purpose of this study was to explore the underlying mechanisms by which BMSCs modulate the function of activated HSCs.
Methods
We used BMSCs directly and indirectly co-culture system with HSCs to evaluate the anti-fibrosis effect of BMSCs. Cell proliferation and activation were examined in the presence of BMSCs and HGF. c-met was knockdown in HSCs to evaluate the effect of HGF secreted by BMSCs. The TLR4 and Myeloid differentiation primary response gene 88(MyD88) mRNA levels and the NF-kB pathway activation were determined by real-time PCR and western blotting analyses. The effect of BMSCs on HSCs activation was investigated in vitro in either MyD88 silencing or overexpression in HSCs. Liver fibrosis in rats fed CCl4 with and without BMSCs supplementation was compared. Histopathological examinations and serum biochemical tests were compared between the two groups.
Results
BMSCs remarkably inhibited the proliferation and activation of HSCs by interfering with LPS-TLR4 pathway through a cell–cell contact mode that was partially mediated by HGF secretion. The NF-kB pathway is involved in HSCs activation inhibition by BMSCs. MyD88 over expression reduced the BMSC inhibition of NF-kB luciferase activation. BMSCs protected liver fibrosis in vivo.
Conclusion
BMSCs modulate HSCs in vitro via TLR4/MyD88/NF-kB signaling pathway through cell–cell contact and secreting HGF. BMSCs have therapeutic effects on cirrhosis rats. Our results provide new insights into the treatment of hepatic fibrosis with BMSCs.
doi:10.1371/journal.pone.0043408
PMCID: PMC3426540  PMID: 22927965

Results 1-3 (3)