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C-X-C chemokine receptor type 5+CD8+T cells as immune regulators in hepatitis Be antigen-positive chronic hepatitis B under interferonalpha treatment

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World Journal of Gastroenterology 2025年第3期31卷 73-83页

作者： Zhen-Yu Xu Zhong-Shang Dai Guo-Zhong Gong Min Zhang Department of infectious {1. Second Xiangya HospitalCentral South UniversityChangsha 410011Hunan ProvinceChina Institute of Hepatology and Department of infectious {1. The Second Xiangya HospitalCentral South UniversityChangsha 410011Hunan ProvinceChina

BACKGROUND C-X-C chemokine receptor type 5(CXCR5)+CD8+T cells represent a unique immune subset with dual roles,functioning as cytotoxic cells in persistent viral infections while promoting B cell *** their importance,the specific role of CXCR5+CD8+T cells in chronic hepatitis B(CHB),particularly during interferon-alpha(IFN-α)treatment,is not fully *** study aims to elucidate the relationship between CXCR5+CD8+T cells and sustained serologic response(SR)in patients undergoing 48 weeks of pegylated IFN-α(peg-IFN-α)treatment for *** To elucidate the relationship between CXCR5+CD8+T cells and sustained SR in patients undergoing 48 weeks of peg-IFN-αtreatment for *** This study enrolled 60 patients with hepatitis Be antigen(HBeAg)-positive CHB undergoing 48 weeks of peg-IFN-α*** were assessed for eligibility based on criteria such as persistent HBsAg-positive status for at least six months,HBeAb-negative,hepatitis B virus DNA levels exceeding 2×1.4 copies/mL,and alanine aminotransferase(ALT)levels between 2 and 1. times the upper limit of *** samples were collected at baseline and at weeks 1.,24,48,and a 24-week treatment-free follow-up(week 72)to measure serum interleukin(IL)-21.concentration via ELISA and to analyze CXCR5 and programmed death-ligand 1.PD-L1.expression on CD8+T cells by flow cytometry,CXCR5 is a chemokine receptor that directs immune cells to specific tissues,while PD-L1.is a protein that regulates immune responses by inhibiting T cell *** Patients with CHB exhibited significantly lower levels of circulating CXCR5+CD8+T cells compared to healthy controls(P1..Notably,CXCR5+CD8+T cells were prominently expressed in patients who achieved sustained SR compared to non-SR(NSR).A significant correlation was observed between CXCR5 and PD-L1.expression(r=-0.1.9,P=0.002).However,there was no significant correlation between serum IL-21.levels and CXCR5+CD8+lymphocytes(r=-0.03,P=0.62

关键词： C-X-C chemokine receptor type 5 Programmed death-ligand 1 Interleukin-21 Pegylated interferon-alpha Chronic hepatitis B

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Comparison and significance of specific and non-specific cellular immunity in patients with chronic hepatitis B caused by infection with genotypes B or C of hepatitis B virus

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Science China(Life Sciences) 2009年第8期52卷 719-723页

作者： GU XiBing,YANG XiaoJuan,WANG Dong,HUA Zhong,WU HangYuan,CHEN HaoKun,XU YueQin & LU ZhongHua wuxi {1. for infectious diseases,wuxi 21.005,China 1. wuxi hospital for infectious diseases Wuxi 214005 China

The present study was designed to investigate possible relationships between the genotypes of hepatitis B virus(HBV) and the HBV-specific cytotoxic T lymphocyte(CTL) *** genotypes,HBV specific CTL HBV DNA and other markers of HBV infection were determined in 1.8 patients with chronic hepatitis *** results showed that the patients infected with genotype C(n=62) had a significantly lower HBV-specific CTL response than those who were infected with HBV genotype B(P1..HBV DNA titer was higher in patients infected with HBV genotype C than in those infected with HBV geno-type B(P1..Both alanine aminotransferase(ALT) and total bilirubin(TBIL) were higher in HBV genotype C infected patients than in those infected with genotype B(P1.and <0.05,respectively).These results suggest that compared with CHB patients infected with HBV genotype B,the higher HBV DNA level and more severe liver damages in the patients infected with genotype C of HBV may be associated with genotype C of the virus.

关键词： chronic hepatitis B hepatitis B virus(HBV) genotypes specific cytotoxic T lymphocyte

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Gut microbiota shifts in hepatitis B-related portal hypertension after transjugular intrahepatic portosystemic shunt:Mechanistic and clinical implications

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World Journal of Gastroenterology 2025年第3期31卷 134-137页

作者： Qi-Rong Jiang Da-Wu Zeng Department of Hepatology Hepatology Research InstituteThe First Affiliated HospitalFujian Medical UniversityFuzhou 350005Fujian ProvinceChina Department of infectious {1. The First Affiliated Hospital of Fujian Medical UniversityFuzhou 350004Fujian ProvinceChina

In this article,we provide commentary on the recent article by Zhao et *** focus on the shifts in the gut microbiota of patients with hepatitis B virus(HBV)-associated cirrhosis/portal hypertension(PH)following transjugular intrahepatic portosystemic shunt(TIPS)and the implications for understanding the mechanisms,diagnosis,and *** comparing the gut microbiota composition and dynamic changes before and after TIPS in patients with and without hepatic encephalopathy,the authors found an increase in non-probiotic bacteria in those who developed hepatic encephalopathy post-TIPS,with Morganella species present only in the hepatic encephalopathy *** gut microbiota changes post-TIPS among patients without the occurrence of hepatic encephalopathy suggest potential therapeutic benefits through prophylactic microbiome ***,the specific gut microbiota alterations may hold promise to predict the risk of hepatic encephalopathy in individuals undergoing TIPS for HBVrelated *** these promising findings,future studies are needed to address limitations,including a small sample size,a relatively short evaluation period for gut microbiota alterations,the absence of data on dynamic alterations in gut microbiota post-TIPS and their correlation with blood ammonia levels,and the lack of validation in animal *** conclusion,Zhao et al's study has shed new light on the link of gut microbiota with post-TIPS hepatic encephalopathy,potentially through the intricate gut-liver axis,and has important clinical implications for improving the management of patients with HBV-related PH.

关键词： Hepatitis B virus Cirrhosis Portal hypertension Hepatic encephalopathy Transjugular intrahepatic portosystemic shunt Gut microbiota

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Interleukin-1.A facilitates tumor progression via upregulating programmed death ligand-1.expression in hepatocellular carcinoma

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World Journal of Gastrointestinal Oncology 2025年第1期17卷 176-198页

作者： Zhong-Xia Yang Li-Ting Zhang Xiao-Jun Liu Xue-Bin Peng Xiao-Rong Mao The First School of Clinical Medicine Lanzhou UniversityLanzhou 730000Gansu ProvinceChina Department of infectious {1. The First Hospital of Lanzhou UniversityLanzhou 730000Gansu ProvinceChina Department of Radiotherapy Gansu Provincial HospitalLanzhou 730000Gansu ProvinceChina

BACKGROUND Hepatocellular carcinoma(HCC)is an inflammation-associated tumor with a dismal *** has become an important treatment strategy for HCC,as immunity is closely related to inflammation in the tumor *** regulates the expression of programmed death ligand-1.PD-L1.in the immunosuppressive tumor microenvironment and affects im-munotherapy ***-1.A(IL-1.A)is involved in the remodeling of the tumor microenvironment and plays a protumor or antitumor role in different *** hypothesized that IL-1.A participates in tumor progression by affe-cting the level of immune checkpoint molecules in *** upregulation of PD-L1.expression in HCC cells by IL-1.A was assessed by reverse transcription PCR,western blotting,and flow *** studies were conducted with gene knockout models and pathway *** function of IL-1.A in immune evasion was explored through coculture of T cells and HCC *** effects of IL-1.A on the malignant biological behaviors of HCC cells were evaluated in vitro,and the antitumor effects of an IL-1.A inhibitor and its synergistic effects with a PD-L1.inhibitor were studied in *** IL-1.A upregulated PD-L1.expression in HCC cells in a dose-dependent manner,whereas IL-1.A receptor knockout or treatment with a small mothers against decapentaplegic 2 inhibitor diminished the PD-L1.expression induced by ***-1.A enhanced the survival of HCC cells in the coculture ***-1.A increased the viability,G2/M ratio,and migration of HCC cells and decreased the apoptotic *** D1.VEGF,MMP9,and Bcl-1.expression increased after IL-1.A treatment,whereas BAX expression *** combination of IL-1.A and PD-L1.inhibitors showed synergistic antitumor efficacy and increased cluster of differentiation 8+T lymphocyte infiltration in an HCC mouse *** IL-1.A upregulates PD-L1.expression via the IL-1.A receptor/phosphorylation-small mothers against

关键词： Interleukin-1.A Programmed death ligand-1 Interleukin-1.A receptor Small mothers against decapentaplegic 2 Hepatocellular carcinoma Immunotherapy

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Transforming growth factor-beta 1.enhances discharge activity of cortical neurons

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Neural Regeneration Research 2025年第2期20卷 548-556页

作者： Zhihui Ren Tian Li Xueer Liu Zelin Zhang Xiaoxuan Chen Weiqiang Chen Kangsheng Li Jiangtao Sheng Department of Microbiology and Immunology Guangdong Provincial Key Laboratory of Infectious Diseases and Molecular ImmunopathologyShantou University Medical CollegeShantouGuangdong ProvinceChina Department of Neurosurgery First Affiliated Hospital of Shantou University Medical CollegeShantouGuangdong ProvinceChina

Transforming growth factor-beta 1.TGF-β1.has been extensively studied for its pleiotropic effects on central nervous system *** neuroprotective or neurotoxic effects of TGF-β1.in specific brain areas may depend on the pathological process and cell types ***-gated sodium channels(VGSCs)are essential ion channels for the generation of action potentials in neurons,and are involved in various neuroexcitation-related ***,the effects of TGF-β1.on the functional properties of VGSCs and firing properties in cortical neurons remain *** this study,we investigated the effects of TGF-β1.on VGSC function and firing properties in primary cortical neurons from *** found that TGF-β1.increased VGSC current density in a dose-and time-dependent manner,which was attributable to the upregulation of Nav1.3 *** VGSC current density and Nav1.3 expression were significantly abolished by preincubation with inhibitors of mitogen-activated protein kinase kinase(PD98059),p38 mitogen-activated protein kinase(SB203580),and Jun NH2-terminal kinase 1.2 inhibitor(SP6001.5).Interestingly,TGF-β1.significantly increased the firing threshold of action potentials but did not change their firing rate in cortical *** findings suggest that TGF-β1.can increase Nav1.3 expression through activation of the ERK1.2-JNK-MAPK pathway,which leads to a decrease in the firing threshold of action potentials in cortical neurons under pathological ***,this contributes to the occurrence and progression of neuroexcitatory-related diseases of the central nervous system.

关键词： central nervous system cortical neurons ERK firing properties JNK Nav1.3 p38 transforming growth factor-beta 1 traumatic brain injury voltage-gated sodium currents

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New role and molecular mechanism of Gadd45a in hepatic fibrosis

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World Journal of Gastroenterology 2016年第9期22卷 2779-2788页

作者： Liang Hong Qing-Feng Sun Ting-Yan Xu Yang-He Wu Hui Zhang Rong-Quan Fu Fu-Jing Cai Qing-Qing Zhou Ke Zhou Qing-Wei Du Dong Zhang Shuang Xu Ji-Guang Ding Department of infectious {1. the Third Affiliated Hospital to Wenzhou Medical University Department of infectious {1. The First Peoples Hospital of Xiaoshan Disrict Department of infectious {1. Tianjin Baodi Hospital

AIM: To investigate the role of Gadd45a in hepatic fibrosis and the transforming growth factor (TGF)-beta/ Smad signaling pathway. METHODS: Wild-type male BALB/c mice were treated with CCl4 to induce a model of chronic liver injury. Hepatic stellate cells (HSCs) were isolated from the liver of BALB/c mice and were treated with small interfering RNAs (siRNAs) targeting Gadd45a or the pcDNA3.1.Gadd45a recombinant plasmid. Cellular alpha-smooth muscle actin (alpha-SMA), beta-actin, type I collagen, phospho-Smad2, phospho-Smad3, Smad2, Smad3, and Smad4 were detected by Western blots. The mRNA levels of alpha-SMA, beta-actin, and type I collagen were determined by quantitative real-time (qRT)-PCR analyses. Reactive oxygen species production was monitored by flow cytometry using 2,7-dichlorodihydrofluorescein diacetate. Gadd45a, Gadd45b, anti-Gadd45g, type I collagen, and SMA local expression in liver tissue were measured by histologic and immunohistochemical analyses. RESULTS: Significant downregulation of Gadd45a, but not Gadd45b or Gadd45g, accompanied by activation of the TGF-beta/Smad signaling pathways was detected in fibrotic liver tissues of mice and isolated HSCs with chronic liver injury induced by CCl4 treatment. Overexpression of Gadd45a reduced the expression of extracellular matrix proteins and alpha-SMA in HSCs, whereas transient knockdown of Gadd45a with siRNA reversed this process. Gadd45a inhibited the activity of a plasminogen activator inhibitor-1.promoter construct and (CAGA)(9) MLP-Luc, an artificial Smad3/4-specific reporter, as well as reduced the phosphorylation and nuclear translocation of Smad3. Gadd45a showed protective effects by scavenging reactive oxygen species and upregulating antioxidant enzymes. CONCLUSION: Gadd45a may counteract hepatic fibrosis by regulating the activation of HSCs via the inhibition of TGF-beta/Smad signaling.

关键词： Antioxidant Gadd45a Hepatic fibrosis Hepatic stellate cells Transforming growth factor-beta/Smad signaling

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Prostaglandin E1.protects hepatocytes against endoplasmic reticulum stress-induced apoptosis via protein kinase A-dependent induction of glucose-regulated protein 78 expression

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World Journal of Gastroenterology 2017年第40期23卷 7253-7264页

作者： Fang-Wan Yang Yu Fu Ying Li Yi-Huai He Mao-Yuan Mu Qi-Chuan Liu Jun Long Shi-De Lin Department of infectious {1. Affiliated Hospital of Zunyi Medical College Department of infectious {1. Heze Municipal Hospital

AIM To investigate the protective effect of prostaglandin E1.PGE1. against endoplasmic reticulum(ER) stressinduced hepatocyte apoptosis, and to explore its underlying *** Thapsigargin(TG) was used to induce ER stress in the human hepatic cell line L02 and hepatocarcinomaderived cell line Hep G2. To evaluate the effects of PGE1.on TG-induced apoptosis, PGE1.was used an hour prior to TG treatment. Activation of unfolded protein response signaling pathways were detected by western blotting and quantitative real-time RTPCR. Apoptotic index and cell viability of L02 cells and Hep G2 cells were determined with flow cytometry and MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2 H-tetrazolium] assay. RESULTS Pretreatment with 1.μmol/L PGE1.protected against TG-induced apoptosis in both L02 cells and Hep G2 cells. PGE1.enhanced the TG-induced expression of C/EBP homologous protein(CHOP), glucose-regulated protein(GRP) 78 and spliced X box-binding protein 1.at 6 h. However, it attenuated their expressions after 24 h. PGE1.alone induced protein and m RNA expressions of GRP78; PGE1.also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phosphoeukaryotic initiation factor 2α and CHOP. Treatment with protein kinase A(PKA)-inhibitor H89 or KT5720 blocked PGE1.induced up-regulation of GRP78. Further, the cytoprotective effect of PGE1.on hepatocytes was not observed after blockade of GRP78 expression by H89 or small interfering RNA specifically targeted against human *** Our study demonstrates that PGE1.protects against ER stress-induced hepatocyte apoptosis via PKA pathwaydependent induction of GRP78 expression.

关键词： Hepatocytes Endoplasmic reticulum stress Thapsigargin Glucose-regulated protein 78 Protein kinase A Apoptosis

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Sodium butyrate protects against toxin-induced acute liver failure in rats

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Hepatobiliary & Pancreatic diseases International 2014年第3期13卷 309-315页

作者： Fan Yang Li-Kun Wang Xun Li Lu-Wen Wang Xiao-Qun Han Zuo-Jiong Gong Department of infectious {1. Renmin Hospital of Wuhan University Department of infectious {1. Linyi People's Hospital

BACKGROUND: Acute liver failure(ALF) is a serious clinical syndrome with high mortality. Sodium butyrate has been shown to alleviate organ injury in a wide variety of preclinical models of critical diseases. The aim of this study was to investigate the protective effect of sodium butyrate on ALF in ***: All rats were randomly divided into control,model and sodium butyrate treatment groups. Except the control group, the rats were induced ALF animal model by subcutaneous injection of human serum albumin+D- galactosamine+lipopolysaccharide. After induction of ALF,the rats in the treatment group received sodium butyrate(500mg/kg) at 1.-hour or 24-hour time point. Fourty-eight hours after ALF induction, the animals were sacrificed and samples were harvested. Serum endotoxin, high mobility group box-1.HMGB1., liver function parameters, tumor necrosis factoralpha(TNF-α) and interferon-gamma(IFN-γ) were *** expression of HMGB1.and nuclear factor-kappa B(NF-κB)p65 protein in liver tissue was detected by Western blotting. The histological changes of liver and intestine were examined. The survival duration was also ***: Serum endotoxin, alanine aminotransferase, HMGB1.TNF-α and IFN-γ were significantly increased and the liver histology showed more severe histopathological injury in the model group compared with the control group(P1.and NF-кB p65 proteins in liver tissue, and prolonged the survival duration regardless of treatment at 1. hours or 24 hours after induction of ALF(P<0.05).CONCLUSIONS: Sodium butyrate protected the liver from toxin-induced ALF in rats. The mechanisms may be due to direct hepatoprotection and decreased intestinal permeability.

关键词： acute liver failure high mobility group box-1 nuclear factor-kappa B p65 animal model sodium butyrate

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Histone deacetylase inhibitor suberoylanilide hydroxamic acid alleviates liver fibrosis by suppressing the transforming growth factor-β1.signal pathway

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Hepatobiliary & Pancreatic diseases International 2018年第5期17卷 423-429页

作者： Yao Wang Lei Zhao Fang-Zhou Jiao Wen-Bin Zhang Qian Chen Zuo-Jiong Gong Department of infectious {1. Renmin Hospital of Wuhan University Department of infectious {1. Union Hospital Tongji Medical College Huazhong University of Science and Technology

Background: Histone deacetylases(HDACs) inhibitors are new anti-fibrotic drugs that inhibit the activity of hepatic stellate cells. The present study focused on the anti-fibrotic function of HDAC inhibitor suberoylanilide hydroxamic acid(SAHA) by suppressing transforming growth factor-β1.TGF-β1. signaling. Methods: Male Sprague-Dawley rats were used to induce liver fibrosis with carbon tetrachloride(CCl 4) and LX2 cell(human hepatic stellate cell line) was stimulated by TGF-β1. Both animals and cells were treated with SAHA. The Smad7 and connective tissue growth factor(CTGF) mRNA levels were detected by real-time polymerase chain reaction(PCR). Western blotting was used to examine the protein levels of CTGF, Histone H3(H3), Smad7, Smad2/3, Acetyl-Histone H3(AH3), HDAC2, α-smooth muscle actin( α-SMA), HDAC6, p-Smad2/3 and HDAC8. In addition, the TGF-β1.and liver enzyme levels from rat serum were detected. Histopathological changes were examined by hematoxylin and eosin(HE), Sirius red and Masson trichrome staining. The α-SMA expression was detected by immumohistochemical staining. Results: Compared with control group, the TGF-β1.and liver enzyme levels from rat serum, together with the mRNA levels of CTGF and protein levels of CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were elevated in fibrotic rats( P 1.. But the Smad7 mRNA and AH3 protein levels were notably suppressed in the fibrotic rats( P 1.. Pathological examination showed the typical changes of liver fibrosis in the fibrotic rats. After the treatment with SAHA, the levels of liver enzymes, TGF-β1. CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were reduced( P 1. and Smad7 and AH3 protein contents were elevated in liver fibrotic rats( P 1.. Moreover, immumohistochemistry showed that SAHA significantly suppressed the α-SMA protein content in fibrotic liver( P 1.. Conclusion: The HDAC inhibitor SAHA alleviated liver fibrosis by suppressing the TGF-β1.signaling.

关键词： Acetylation Transforming growth factor-β1 Liver fibrosis Suberoylanilide hydroxamic acid

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Effect of medical ozone therapy on renal blood flow and renal function of patients with chronic severe hepatitis

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Chinese Medical Journal 2010年第18期123卷 2510-2513页

作者： GU Xi-bing YANG Xiao-juan ZHU Hong-ying XU Yue-qin LIU Xia-ying Department of Liver diseases Wuxi Hospital for Infectious Diseases Wuxi Jiangsu 214005 China

Background Medical ozone therapy system was reported to have certain effects on the treatment of severe hepatitis, but its mechanism is not very clear. One of the causes of death of severe hepatitis is complication of renal damage or hepatorenal syndrome. The present study aimed to observe effects of medical ozone therapy system on plasma renin activity （PRA）, angiotensin II （All）, aldosterone （ALD）, renal blood flow and renal function of patients with chronic severe hepatitis and explore mechanisms of medical ozone therapy in the treatment of severe hepatitis. Methods Eighty-five cases with chronic severe hepatitis were randomly divided into ozone therapy group （43 cases） and control group （42 cases）. The patients in the ozone therapy group were treated with basic treatments plus ozone therapy system. Basic autohemotherapy was used. One hundred milliliter venous blood was drawn from each patient, and was mixed with 1.0 ml （35 pg/ml） medical ozone and then was returned the blood to the patient intravenously, once every other day for 20 days. Only the basic treatments were given to the control group. PRA, All, ALD, renal blood flow and damage to renal function of the two groups before treatment and 20 days after treatment were compared. Survival rates were also compared. Results Twenty days after the treatment, in ozone therapy group, PRA was （1.31.0.1.） ng.m^-1.h^1. All （1.1.25±1..35） pg/ml, ALD （251.31.22.60） pg/ml, which decreased significantly compared with those before treatment （PRA （2.23±0.1.） ***^-1.h^-1. All （1.5.1.±1..1.） pg/ml, ALD （405.31.29.88） pg/ml, t=4.67-1..23, P 〈0.01.）, also lower than those of control group 20 days after the treatment （PRA （2.02±0.1.） ***^-1.h^-1. All （1.2.21.1..32） pg/ml, ALD （401.20±35.02） pg/ml, t=4.97-1..61. P 〈0.01.; renal blood flow was （1.5.1.±28.20） ml/min, which increased compared with that before the treatment （（1.5.68±21.25） ml/min） and was higher than that of control group 20 days after the treatment （（1.8.59±23.1.

关键词： medical ozone chronic severe hepatitis renal blood flow

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