scholarly journals Serum IL-33 Levels Are Associated with Liver Damage in Patients with Chronic Hepatitis C

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Juan Wang ◽  
Pingwei Zhao ◽  
Hui Guo ◽  
Xiguang Sun ◽  
Zhenyu Jiang ◽  
...  

Interleukin-33 (IL-33) is associated with the development of Th2 responses. This study examined the potential role of IL-33 in the pathogenic process of chronic hepatitis C (CHC) in Chinese patients. The levels of serum IL-33 and sST2 in 154 patients with CHC, 24 with spontaneously resolved HCV (SR-HCV) infection and 20 healthy controls (HC), were analyzed by ELISA. The concentrations of serum IL-2, IFN-γ, TNF-α, IL-4, IL-6, and IL-10, HCV loads, ALT, AST, and HCV-Ab were measured. We found that the levels of serum IL-33 in CHC patients were significantly higher than those of SR-HCV and HC but decreased after treatment with interferon for 12 weeks. More importantly, the levels of serum IL-33 were correlated with the concentrations of ALT and AST in CHC patients. The levels of serum sST2, as a decoy receptor of IL-33, were significantly higher in CHC and SR-CHC patients than those in HC, and there was no correlation between the levels of serum sST2 and IL-33. The concentrations of serum IFN-γ and IL-6 in CHC patients were significantly lower than those of SR-HCV. These data suggest that IL-33 may be a pathogenic factor contributing to CHC-related liver injury.

2008 ◽  
Vol 83 (2) ◽  
pp. 836-846 ◽  
Author(s):  
Karla J. Helbig ◽  
Andrew Ruszkiewicz ◽  
Robert E. Lanford ◽  
Mark D. Berzsenyi ◽  
Hugh A. Harley ◽  
...  

ABSTRACT To investigate chemokine expression networks in chronic hepatitis C virus (HCV) infection, we used microarray analysis to determine chemokine expression in human infection and in chimpanzees experimentally infected with HCV. The CXCR3 chemokine family was highly expressed in both human and chimpanzee infection. CXCL10 was the only CXCR3 chemokine elevated in the serum, suggesting that it may neutralize any CXCR3 chemokine gradient established between the periphery and liver by CXCL11 and CXCL9. Thus, CXCR3 chemokines may not be responsible for recruitment of T lymphocytes but may play a role in positioning these cells within the liver. The importance of the CXCR3 chemokines, in particular CXCL11, was highlighted by replicating HCV (JFH-1) to selectively upregulate its expression in response to gamma interferon (IFN-γ) and tumor necrosis factor alpha (TNF-α). This selective upregulation was confirmed at the transcriptional level by using the CXCL11 promoter driving the luciferase reporter gene. This synergistic increase in expression was not a result of HCV protein expression but the nonspecific innate response to double-stranded RNA (dsRNA), as both in vitro-transcribed HCV RNA and the dsRNA analogue poly(I:C) increased CXCL11 expression and promoter activity. Furthermore, we show that CXCL11 is an IRF3 (interferon regulatory factor 3) response gene whose expression is selectively enhanced by IFN-γ and TNF-α. In conclusion, the CXCR3 chemokines are the most significantly expressed chemokines in chronic hepatitis C and most likely play a role in positioning T cells in the liver. Furthermore, HCV can selectively increase CXCL11 expression in response to IFN-γ and TNF-α stimulation that may play a role in the pathogenesis of HCV-related liver disease.


2000 ◽  
Vol 20 (4) ◽  
pp. 305-311 ◽  
Author(s):  
Mitsuo Toyoda ◽  
Satoru Kakizaki ◽  
Norio Horiguchi ◽  
Ken Sato ◽  
Hisashi Takayama ◽  
...  

Hepatology ◽  
2005 ◽  
Vol 42 (4) ◽  
pp. 975-976 ◽  
Author(s):  
Robert F. Schwabe ◽  
Soeren V. Siegmund

2021 ◽  
Vol 2 (2) ◽  
Author(s):  
Yuanjiang Liu

Objective — To analyze and study the predict value of serum levels of RNA-dependent protein kinase (PKR), tumor necrosis factor alpha (TNF-α), interleukin 10 (IL-10) and interferon gamma (INF-γ) for HCV clearance in patients with HCV infection. Methods — A total of 92 patients with chronic HCV infection (case group), 33 patients with HCV spontaneous resolvers (SR group) and 100 healthy persons (control group) during the same period from January 2018 to October 2019 in our hospital's infection department were collected as the study Object. The basic data and routine biochemical indicators of the three groups of subjects were detected and compared, and the levels of serum PKR, TNF-α, INF-γ and IL-10 were detected by enzyme-linked immunosorbent assay. The ROC work curve analysis was used to evaluate the predictive value of the above immune indicators for HCV clearance in patients with hepatitis C. Results — Compared with the control group and the case group, the serum PKR, TNF-α and IFN-γ levels in the SR group increased, while the IL-10 levels decreased, the difference was statistically significant. Predictive analysis of HCV clearance in chronic hepatitis C patients found that the area under the ROC curve of PKR and IFN-γ were 0.784 (95% CI: 0.704-0.864, P <0.001) and 0.645 (95% CI: 0.538-0.751, P = 0.014), and the optimal cut-off points are 7.00 ng / mL and 101.00 pg / mL, respectively. Conclusion — Both PKR and IFN-γ have a certain predictive value for the clearance of HCV in patients with chronic hepatitis C, which can be used as a potential biomarker for predicting the outcome of HCV infection.


2017 ◽  
Vol 30 (1) ◽  
pp. 249
Author(s):  
EsraaE Elmahdy ◽  
AhmedA Salama ◽  
NahedA El-Ragehy ◽  
AtefA Ali

2006 ◽  
Vol 26 (7) ◽  
pp. 817-826 ◽  
Author(s):  
Athanassios C. Tsamandas ◽  
Ioulia Syrokosta ◽  
Konstantinos Thomopoulos ◽  
Vassiliki Zolota ◽  
Dimitra Dimitropoulou ◽  
...  

2021 ◽  
Author(s):  
Daniela Alejandra Rios ◽  
Paola Cecilia Casciato ◽  
María Soledad Caldirola ◽  
María Isabel Gaillard ◽  
Cecilia Giadans ◽  
...  

Abstract Background: Chronic hepatitis C pathogenesis is not defined yet, so immune cell populations and cytokines in liver and peripheral blood (PB) were evaluated to elucidate their role in liver disease. B, CTL, Th, Treg, Th1, Th17 and NK cells localization and frequency were evaluated on liver biopsies by immunohistochemistry, while frequency, differentiation, and functional status on PB by flow cytometry. TNF−α, IL−23, IFN−γ, IL−1β, IL−6, IL−8, IL−17A, IL−21, IL−10 and TGF−β expression were quantified in fresh liver biopsy by RT-qPCR and in plasma by CBA/ELISA. Results: Liver CTL and Th1 at lobular area inversely correlated with viral load (r=−0.469, p=0.003 and r=−0.384, p=0.040). Treg correlated with CTL and Th1 at lobular area (r=0.784, p<0.0001; r=0.436, p=0.013). Th17 correlated with hepatic IL-8 (r=0.52, p<0.05) and both were higher in advanced fibrosis cases (Th17 p=0.0312, IL-8 p=0.009). Hepatic cytokines were higher in severe hepatitis cases (IL−1β p=0.026, IL−23 p=0.031, IL−8 p=0.002, TGF−β p=0.037). Peripheral NK (p=0.008) and NK Dim (p=0.018) were diminished while NK Bright (p=0.025) were elevated in patients vs donors. Naïve Th (p=0.011) and CTL (p=0.0007) were decreased, while activated Th (p=0.0007) and CTL (p=0.0003) were increased. IFN−γ production and degranulation activity in NK and CTL were normal. Peripheral cytokines showed an altered profile, particularly elevated IL−6 (p=0.008) and TGF−β (p=0.041). Conclusions: HCV-specific and non-specific hepatic CTLs favored damage. Treg could not prevent fibrogenesis triggered by Th17 and IL-8. Peripheral T-lymphocyte differentiation stages shift, elevated cytokines levels and NK-cell count decrease would contribute to global disease.


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