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Objective:To explore the possible correlation between serum detection of IL-7, IL-21, HBV-specific cytotoxic T lymphocytes (CTLs), HBV DNA, and the expression of CD127 on the T lymphocytes, and discuss the effect of IL-7 to cellular immune response in patients with chronic hepatitis B (CHB).Methods:Five hundred and sixty serum samples were collected from patients with CHB in Beijing Friendship Hospital from September 2017 to March 2020. The serum IL-7 and IL-21 were detected by enzyme-linked immunosorbent assay (ELISA), and HBV-specific CTLs and the expression of CD127 on the T lymphocytes were determined by flow cytometry. While HBV DNA were tested using quantitative real-time PCR (qRT-PCR). Subjects were divided into groups A, B, and C, according to the IL-7 levels (low: IL-7<20 pg/ml, medium: 20 pg/ml≤IL-7<30 pg/ml, and high: IL-7≥30 pg/ml).Results:The average concentration of serum IL-7 in patients with CHB was significantly lower than that of healthy controls ( P<0.01), and the difference among three groups was statistically significant ( P<0.01). Meanwhile, levels of IL-21, percentages of HBV-specific CTL, and the expression of CD127 on the CD8 + T lymphocytes showed an upward trend among groups, and there were significant differences among three groups ( P<0.01) with a positive correlation between each two variables ( P<0.01). However, HBV DNA showed a downward trend in group A, B and C, and the difference of the three groups were statistically significant ( P<0.01), which were negatively correlated with other variables ( P<0.01). Multiple linear regression analysis showed that HBV-specific CTL was an independent influencing factor for HBV DNA ( P<0.01), and IL-7, the expression of CD127 on the CD8 + T lymphocytes and IL-21 had an independent effect on HBV-specific CTL ( P<0.05). Conclusions:IL-7 could regulate HBV-specific immune response, and might be used as an effective cellular immune indicator to evaluate the cellular immune status of patients with chronic hepatitis B.
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Objective:To investigate the correlation of serum hepatitis B virus large protein (HBV-LP), HBV-DNA, and Pre S1 antigen (Pre S1-Ag) with HBV replication.Methods:Serum samples were collected from 650 patients with chronic hepatitis B (CHB) who were treated in Beijing Friendship Hospital from March 2017 to March 2019. Serum HBV-LP and Pre S1-Ag were detected by enzyme-linked immunosorbent assay (ELISA). HBV markers (HBV-M) were measured using chemiluminescent microparticle immunoassay (CMIA). Quantitative real-time PCR (qRT-PCR) was used to detect HBV-DNA. The positive detection rates of HBV-DNA, HBV-LP and Pre S1-Ag were calculated and compared, and the correlation of HBV-LP (S/CO value) and hepatitis B surface antigen (HBsAg, log 10 IU/ml) with HBV-DNA(log 10 IU/ml)was analyzed. Results:In the 650 CHB patients, the positive rates of HBV-DNA, HBV-LP and Pre S1-Ag were 65.4% (425/650), 79.2% (515/650) and 43.1% (280/650), respectively ( P<0.01). The positive rates of HBV-DNA and HBV-LP in 243 HBeAg-positive patients were 93.0% (226/243) and 94.6% (230/243), and no significant difference was found between them ( P=0.45). However, there was significant difference between the positive rates of HBV-DNA and HBV-LP in 407 patients negative for HBeAg [48.9% (199/407) vs 70.0% (285/407), P<0.01]. The positive rates of HBV-DNA and HBV-LP in HBsAg-, HBeAg- and HBcAb-positive groups were 92.8% (206/222) and 94.1% (209/222), which showed no significant difference ( P=0.56). In HBsAg-, HBeAb- and HBcAb-positive groups, the positive rates of HBV-DNA and HBV-LP were 45.4% (124/273) and 69.9% (191/273) ( P<0.01). The detection rate of HBeAg was lower than that of HBV-LP significantly in both HBV-DNA-positive and HBV-DNA-negative groups ( P<0.01). With the increasing of HBV-DNA load, the S/CO value and the positive rate of HBV-LP increased significantly ( P<0.05). Conclusions:HBV-LP had a good correlation with HBV-DNA load as compared with Pre S1-Ag, HBeAg and HBsAg. HBV-LP in combination with HBV-M might be used as predictive markers that could efficiently reflect the status of HBV replication.
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Objective@#The traditional Chinese medicine Anluohuaxianwan (ALHXW) has been used to treat liver fibrosis induced by chronic hepatitis B virus (HBV) infection. However, the anti-fibrosis mechanisms of ALHXW remain to be investigated. This study used a rat model of carbon tetrachloride (CCl4)-induced liver fibrosis to explore the potential antifibrogenic mechanisms of ALHXW.@*Methods@#Twenty-seven male Wistar rats were randomly assigned to control group, model group, and treatment group (n = 9 per group). Rats in the model and treatment group were injected intraperitoneally with 40% CCl4(2 ml/kg), and rats in the control group were administered saline twice a week for 6 weeks. Starting at week 4 following model construction, rats in the treatment group received daily gavages with ALHXW solution (concentration 0.15 g/ml) daily, while rats in the control and model groups were given saline for a total of 6 weeks. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were measured from blood samples collected at the end of weeks 3, 6 and 9. Histopathological examination of liver tissue was performed to evaluate liver fibrosis at week 9. At the same time, the mRNA expression of TGF-β1 and Smads in liver tissues was quantified by real-time reverse transcription polymerase chain reaction (RT-PCR), and TGF-β1 protein level in the liver was measured by Western blot. Inter-group comparison was performed using analysis of variance (ANOVA) when the continuous data were normally distributed and satisfied the homogeneity of variance; otherwise, nonparametric tests were used. Categorical data were compared between groups using nonparametric tests.@*Results@#ALHXW markedly alleviated liver injury in the treatment group after 3 weeks of therapy as indicated by a significantly reduced level of ALT compared with the model group [(162.98 ± 73.14)U/L vs (322.52 ± 131.76)U/L, P = 0.047], and a 39.8% reduction in AST level compared with the model group[ (537.56 ± 306.06)U/L vs (892.98 ± 358.19)U/L, P = 0.053]. Moreover, at the end of the 6-week therapy, histopathological diagnosis showed that liver fibrosis was significantly reduced in the ALHXW-treated group compared with that in the model group (P = 0.002). The relative expression of TGF-β1 mRNA and protein in the liver were significantly lower in ALHXW-treated rats than that in model rats (1.34 ± 0.31 vs 1.78 ± 0.45, P = 0.025; 0.39 ± 0.02 vs 0.57 ± 0.04, P = 0.003).@*Conclusion@#ALHXW treatment can reverse CCl4-induced liver fibrosis in rats. Its mechanisms of anti-fibrosis may occur through the inhibition of TGF-β1 synthesis and TGF-β1/Smads signaling pathway, which in turn suppress the activation of hepatic stellate cells and thereby reverses fibrosis.