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Objective To investigate the current status of hepatitis B virus (HBV) infection among hospitalized patients aged 1-18 years, as well as the status of immunity after hepatitis B vaccination. Methods Related data were collected from the patients aged 1-18 years who were hospitalized in Henan Provincial People's Hospital from July 2020 to July 2021, including serological markers for hepatitis B (HBsAg, anti-HBs, HBeAg, anti-HBe, and anti-HBc) and hepatitis B vaccination. The epidemiological situation of HBV infection was analyzed, as well as the immune effect after vaccination. The trend chi-square test was used for trend analysis. Results A total of 10 658 hospitalized patients were collected, among whom there were 6 372 male patients (59.79%) and 4 286 female patients (40.21%). In this population, the patients with positive HBsAg accounted for 0.28% (30/10 658), with a relatively high proportion of 0.68% and 0.62%, respectively, in the 17-and 18-year age groups; the patients with positive anti-HBs accounted for 51.82% (5 523/10 658), with a relatively high proportion of > 63% in the 1-4 years age groups, and there was a reduction in the proportion of patients with positive anti-HBs (fluctuating around 40%) in the 5-18 years age groups. With the increase in age, the positive rate of anti-HBs tended to decrease in both male and female patients (male: χ 2 =8.217, P =0.004; female: χ 2 =10.048, P =0.002). Conclusion Based on the data of hospitalized patients, HBV infection in the population aged 1-18 years in Henan Province has the characteristics of low prevalence rate and high immunity, and the reduction in the proportion of patients with positive anti-HBs at more than five years after vaccination should be taken seriously in this region.
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Objective@#To observe ascitic interleukin-7 expression level in cirrhotic patients complicated with spontaneous bacterial peritonitis, and to detect the effect of recombinant human IL-7 on CD4+ and CD8+T lymphocyte function.@*Methods@#A total of 84 patients with liver cirrhosis who were hospitalized from August 2017 to April 2018 were selected. Among them, 51 cases were complicated with cirrhosis and untainted ascites, and 33 cases were cirrhosis complicated with spontaneous bacterial peritonitis. Peripheral blood and ascites were collected routinely. The levels of IL-7 in peripheral blood and ascites were measured by enzyme-linked immunosorbent assay. CD4+T cells and CD8+T cells were purified from ascites, and were stimulated with recombinant IL-7. Cellular proliferation, key transcription factors for mRNA, and cytokines production by CD4+T cells in response to IL-7 stimulation was measured. mRNA expression corresponding to perforin, granzyme B, and granulysin as well as cytokines production by CD8+T cells was also measured in response to IL-7 stimulation. Cytolytic and non-cytolytic activity of CD8+T cells in response to IL-7 stimulation was also investigated in both direct and indirect contact co-culture system. Measurement data of the normal distribution were compared between the two groups by Student’s t-test and the data before and after stimulation were compared by paired t-test. Measurements that did not conform to normal distribution were compared between the two groups using Mann-Whitney U test, and data before and after stimulation were compared using Wilcoxon paired test.@*Results@#There was no significant statistical difference in serum IL-7 levels between the two groups [(5 001 ± 1 458) pg/ml vs. (4 768 ± 1 128) pg/ml, P = 0.41]. The level of ascitic IL-7 in cirrhotic patients complicated with SBP was significantly lower than cirrhosis patients with untainted ascites [(966.4 + 155.8) pg/ml vs. (792.1 + 126.4) pg/ml, P < 0.01]. Recombinant IL-7 stimulation promoted the proliferation of CD4+ and CD8+T cells from ascites in patients with liver cirrhosis complicated by SBP. T-bet mRNA relative expression and IFN-γ secretion in CD4+T cells was also elevated in response to IL-7 stimulation in vitro. Moreover, IL-7 stimulation also increased the mRNA expressions of perforin, granzyme B, and granulysin as well as productions of IFN-γ and TNF-α by CD8+T cells. Recombinant IL-7 stimulation elevated cytolytic and non-cytolytic activity of CD8+T cells from ascites in patients with liver cirrohosis complicated by SBP, which manifested as increased target cell death and IFN-γ production in both direct and indirect contact co-culture system.@*Conclusion@#Ascitic IL-7 promotes T lymphocyte function in patients with liver cirrhosis complicated with SBP.
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Objective@#To investigate the effect of hepatitis B core antigen (HBcAg) in promoting the invasion of hepatitis B virus (HBV)-related hepatocellular carcinoma cell line HepG2.2.15 and the role of Toll-like receptor 4 (TLR4) in the mechanism.@*Methods@#TLR4 mRNA and protein expression in HepG2 cells and HepG2.2.15 cells was measured by reverse transcription real-time PCR and Western blot analysis, respectively. HepG2.2.15 cells were transfected with TLR4 specific small interfering RNA (siRNA) to silence TLR4 expression, and stimulated by recombinant HBcAg in culture. The invasion of cells was measured by Transwell invasion assay. The expression of TLR4 signaling pathway-related proteins in the cultured cells and proinflammatory cytokines in the supernatant was also determined. The student’s t-test, one-way ANOVA, and SNK-q test were used for statistical analysis.@*Results@#TLR4 mRNA and protein expression in HepG2.2.15 cells was significantly higher than that in HepG2 cells. TLR4 siRNA transfection remarkably down-regulated TLR4 expression in HepG2.2.15 cells. Inhibiting TLR4 expression and/or HBcAg stimulation did not affect the proliferation of HepG2.2.15 cells. However, HBcAg stimulation significantly increased the invasion ability of HepG2.2.15 cells and the secretion of proinflammatory cytokines [including interferon (IFN)-γ, interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-α]. Inhibiting TLR4 expression significantly reduced HBcAg-induced cellular invasion. Meanwhile, HBcAg stimulation elevated the expression of MyD88 and TRIF in HepG2.2.15 cells. TLR4 silencing inhibited HBcAg-induced increase in the expression of MyD88, while it showed no significant impact on TRIF expression.@*Conclusion@#HBcAg can promote the invasion of HepG2.2.15 cells. The TLR4/MyD88 signaling pathway may be involved in this process by inducing the expression of proinflammatory cytokines.
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Objective To observe the effect of prostaglandin E1 on soluble interleukin-6 receptor(SIL-6R) and soluble interleukin-6 receptor β strands (sgp 130) in serum in patients with chronic severe hepatitis.Methods Sixteen patients with chronic severe hepatitis accepted therapy with prostaglandin E1.Serum levels of SIL-6R and sgp130 were detected by enzyme linked immunosorbent assay (ELISA) method before and after therapy.Results The content of SIL-6R and sgp 130 in serum were increased significantly (P<0.001) in patients with chronic severe hepatitis compared with normal control group and decreased obviously (P<0.01) after therapy with prostaglandin E1 compared with before therapy,and the rate of delth were decreased obviously (P<0.01) in PGE1 therapy group.Conclusion The levels of SIL-6R and sgp130 in serum can reflect the degree of liver damage in patients with chronic severe hepatitis and guide the assessment of prognosis;PGE1 can correct the immune disorder,attenuating hepatocyte inflammation and necrosis.