To investigate interferon-γ-inducible protein-10’s (IP-10) potential to anticipate rapid (RVR)- and sustained virological responses (SVR) to chronic hepatitis C (CHC) treatment. METHODSWe included case series examin...To investigate interferon-γ-inducible protein-10’s (IP-10) potential to anticipate rapid (RVR)- and sustained virological responses (SVR) to chronic hepatitis C (CHC) treatment. METHODSWe included case series examining RVR or SVR in relation to 24 or 48 wk treatment for CHC, in patients treatment free for at least six months, with genotype 1 or 4, and in relation to 24 wk treatment for genotype 2 and 3, with pegylated interferon in combination with ribavirin. Patients had to have both a baseline IP-10 level as well as a hepatitis C virus (HCV)-RNA determination 4 wk after treatment initiation or 24 wk after end of treatment. Studies including patients with liver diseases other than CHC, human immunodeficiency virus-infection, treatment with immunosuppresents or cytostatica, alcohol dependency or active intravenous drug-use were excluded. We found 81 articles by searching the MEDLINE and EMBASE databases. Eight studies were eligible for inclusion. Their quality were assesed using an 18 point checklist for case series, developed using a modified Delphi technique. Information was extracted from the articles, and no raw data was requisitioned. The review protocol was registered at the International Prospective Register of Systematic Reviews (reg. number: CRD42014008736). RESULTSThree studies reported on baseline IP-10 level in association with RVR. A signigficant association was found for HCV genotype 1 infection by two studies. Only two studies reported on HCV genotype 4 infected and genotype 2 and 3 infected patients, respectively. A trend was seen for an association between RVR and baseline IP-10 for genotype 4, while no association was found for genotype 2 and 3. Seven studies provided information regarding baseline IP-10 and SVR. Following the pattern regarding rapid virological response all five studies examining SVR in relation to baseline IP-10 levels for HCV, genotype 1 infected patients showed a significant association. Likewise a significant association was seen for HCV, genotype 4 infected, while no association was found for HCV, genotype 2 and 3 infected. Though only two studies examined the assosiation for HCV genotype 4 infected and HCV genotype 2 and 3 infected respectively. CONCLUSIONWe found indications of a possible association between baseline IP-10 level and virological responses in patients with CHC genotype 1 and 4.展开更多
变应性气道炎症的免疫失衡受多种免疫因子调节。Th1/Th2失平衡及 Th3细胞的免疫抑制作用是这方面的研究热点。本文主要阐述干扰素-γ诱导的单核因子、单核细胞趋化蛋白-1、转化生长因子-β在变应性气道炎症中的作用机制。了解调节性 T ...变应性气道炎症的免疫失衡受多种免疫因子调节。Th1/Th2失平衡及 Th3细胞的免疫抑制作用是这方面的研究热点。本文主要阐述干扰素-γ诱导的单核因子、单核细胞趋化蛋白-1、转化生长因子-β在变应性气道炎症中的作用机制。了解调节性 T 细胞的免疫调节机制有助于开拓变应性气道炎症治疗的新方法。展开更多
OBJECTIVE:To examine the efficacy of Qinghuayin(清化饮,QHY)in rat chronic atrophic gastritis(CAG)models and explored the molecular mechanism of QHY in treating CAG.METHODS:In total,65 Wistar rats were randomly divided...OBJECTIVE:To examine the efficacy of Qinghuayin(清化饮,QHY)in rat chronic atrophic gastritis(CAG)models and explored the molecular mechanism of QHY in treating CAG.METHODS:In total,65 Wistar rats were randomly divided into the control(n=10)and CAG groups(n=55).CAG model rats were further divided into five groups:model(n=10),vitacoenzyme(n=10),low-dose QHY(n=10),medium-dose QHY(n=10),and high-dose QHY groups(n=10).We analyzed histopathological changes using hematoxylin and eosin staining and measured interleukin(IL)-6 and IL-8 levels in serum using enzyme-linked immunosorbent assay(ELISA)(Boster Bio,Pleasanton,USA).In addition,gastrin(GAS),pepsinogen I(PGI),and PGII expressions were evaluated using ELISA.The protein and m RNA expression of toll-like receptor 4(TLR4)and toll or interleukin-1 receptor domaincontaining adaptor inducing interferon-β(TRIF)was detected by Western blotting and quantitative reverse transcription-polymerase chain reaction,respectively.RESULTS:Our results revealed that histopathological changes in CAG model rates could be restored by low-,medium-,and high-dose QHY.The changes in GAS and PGI/II expression demonstrated that QHY improved CAG.Serum IL-6 and IL-levels were decreased by QHY administration.TLR4 and TRIF were upregulated at the m RNA and protein levels in the model group but downregulated by QHY administration.CONCLUSION:We concluded that QHY could effectively improve the histopathological changes of the gastric mucosa induced by CAG in rats.The therapeutic mechanism of QHY may be related to inhibition of the inflammatory factors IL-6 and IL-8 and suppression of TLR4/TRIF m RNA and protein expression.展开更多
目的分析慢性乙型肝炎(chronic hepatitis B,CHB)HBeAg阳性患者血清干扰素γ诱导单核细胞因子(monokine induced by IFN-γ,Mig)、白细胞介素(interle-ukin,IL)-9与乙型肝炎病毒(hepatitis B Virus,HBV)前C/BCP区变异的相关性以及其对...目的分析慢性乙型肝炎(chronic hepatitis B,CHB)HBeAg阳性患者血清干扰素γ诱导单核细胞因子(monokine induced by IFN-γ,Mig)、白细胞介素(interle-ukin,IL)-9与乙型肝炎病毒(hepatitis B Virus,HBV)前C/BCP区变异的相关性以及其对干扰素疗效影响。方法回顾性分析2015年2月至2018年2月四川省简阳市人民医院收治的110例CHB且HBeAg阳性患者资料,均给予聚乙二醇α-干扰素抗病毒治疗;治疗前扩增患者血清HBV前C/BCP区的基因片段并将患者分成HBV前C/BCP区野生型组(野生组61例)及突变型组(突变组49例),并比较两组患者血清Mig、IL-9情况以及抗病毒治疗疗效差异。结果突变组治疗前患者血清IL-9[(10.8±1.9)ng/L]明显高于野生组[(8.3±1.7)ng/L](P<0.05)。突变组治疗48周后获得完全应答率[46.9%(23/49)]显著高于野生组[16.4%(10/61)]χ^2=7.083,P=0.018;突变组治疗24周后HBsAg下降>1 lg10者较下降≤1 lg10者治疗前的血清Mig显著升高[(129.2±37.9)ng/L与(91.5±25.7)ng/L](P<0.05)。突变组治疗12、24周血清IL-9分别为(8.8±1.9)、(8.9±1.6)ng/L,均较治疗前显著降低(P均<0.05)。结论CHB且HBeAg阳性患者治疗前血清IL-9的高表达与HBV前C/BCP区的变异关系密切,IL-9的表达与干扰素抗病毒疗效无相关性;患者治疗前Mig的高表达可能对HBV前C/BCP区变异者干扰素抗病毒疗效更有利。展开更多
基金Supported by Amagar and Hvidovre Hospital Research Foun-dation of 45000 Dkr.(to Bastian Neesgaard)The Family Hede Nielsen Foundation of 10000 Dkr.(to Bastian Neesgaard)
文摘To investigate interferon-γ-inducible protein-10’s (IP-10) potential to anticipate rapid (RVR)- and sustained virological responses (SVR) to chronic hepatitis C (CHC) treatment. METHODSWe included case series examining RVR or SVR in relation to 24 or 48 wk treatment for CHC, in patients treatment free for at least six months, with genotype 1 or 4, and in relation to 24 wk treatment for genotype 2 and 3, with pegylated interferon in combination with ribavirin. Patients had to have both a baseline IP-10 level as well as a hepatitis C virus (HCV)-RNA determination 4 wk after treatment initiation or 24 wk after end of treatment. Studies including patients with liver diseases other than CHC, human immunodeficiency virus-infection, treatment with immunosuppresents or cytostatica, alcohol dependency or active intravenous drug-use were excluded. We found 81 articles by searching the MEDLINE and EMBASE databases. Eight studies were eligible for inclusion. Their quality were assesed using an 18 point checklist for case series, developed using a modified Delphi technique. Information was extracted from the articles, and no raw data was requisitioned. The review protocol was registered at the International Prospective Register of Systematic Reviews (reg. number: CRD42014008736). RESULTSThree studies reported on baseline IP-10 level in association with RVR. A signigficant association was found for HCV genotype 1 infection by two studies. Only two studies reported on HCV genotype 4 infected and genotype 2 and 3 infected patients, respectively. A trend was seen for an association between RVR and baseline IP-10 for genotype 4, while no association was found for genotype 2 and 3. Seven studies provided information regarding baseline IP-10 and SVR. Following the pattern regarding rapid virological response all five studies examining SVR in relation to baseline IP-10 levels for HCV, genotype 1 infected patients showed a significant association. Likewise a significant association was seen for HCV, genotype 4 infected, while no association was found for HCV, genotype 2 and 3 infected. Though only two studies examined the assosiation for HCV genotype 4 infected and HCV genotype 2 and 3 infected respectively. CONCLUSIONWe found indications of a possible association between baseline IP-10 level and virological responses in patients with CHC genotype 1 and 4.
基金Supported by Natural Science Foundation of Fujian Province(Based on NLRP3 Inflammatory Body/Caspase-1-mediated Gastric Epithelial Cell Death to Explore the Molecular Mechanism of Qinghua Decoction in the Treatment of Chronic Atrophic Gastritis,No.2020J01253)。
文摘OBJECTIVE:To examine the efficacy of Qinghuayin(清化饮,QHY)in rat chronic atrophic gastritis(CAG)models and explored the molecular mechanism of QHY in treating CAG.METHODS:In total,65 Wistar rats were randomly divided into the control(n=10)and CAG groups(n=55).CAG model rats were further divided into five groups:model(n=10),vitacoenzyme(n=10),low-dose QHY(n=10),medium-dose QHY(n=10),and high-dose QHY groups(n=10).We analyzed histopathological changes using hematoxylin and eosin staining and measured interleukin(IL)-6 and IL-8 levels in serum using enzyme-linked immunosorbent assay(ELISA)(Boster Bio,Pleasanton,USA).In addition,gastrin(GAS),pepsinogen I(PGI),and PGII expressions were evaluated using ELISA.The protein and m RNA expression of toll-like receptor 4(TLR4)and toll or interleukin-1 receptor domaincontaining adaptor inducing interferon-β(TRIF)was detected by Western blotting and quantitative reverse transcription-polymerase chain reaction,respectively.RESULTS:Our results revealed that histopathological changes in CAG model rates could be restored by low-,medium-,and high-dose QHY.The changes in GAS and PGI/II expression demonstrated that QHY improved CAG.Serum IL-6 and IL-levels were decreased by QHY administration.TLR4 and TRIF were upregulated at the m RNA and protein levels in the model group but downregulated by QHY administration.CONCLUSION:We concluded that QHY could effectively improve the histopathological changes of the gastric mucosa induced by CAG in rats.The therapeutic mechanism of QHY may be related to inhibition of the inflammatory factors IL-6 and IL-8 and suppression of TLR4/TRIF m RNA and protein expression.
文摘目的分析慢性乙型肝炎(chronic hepatitis B,CHB)HBeAg阳性患者血清干扰素γ诱导单核细胞因子(monokine induced by IFN-γ,Mig)、白细胞介素(interle-ukin,IL)-9与乙型肝炎病毒(hepatitis B Virus,HBV)前C/BCP区变异的相关性以及其对干扰素疗效影响。方法回顾性分析2015年2月至2018年2月四川省简阳市人民医院收治的110例CHB且HBeAg阳性患者资料,均给予聚乙二醇α-干扰素抗病毒治疗;治疗前扩增患者血清HBV前C/BCP区的基因片段并将患者分成HBV前C/BCP区野生型组(野生组61例)及突变型组(突变组49例),并比较两组患者血清Mig、IL-9情况以及抗病毒治疗疗效差异。结果突变组治疗前患者血清IL-9[(10.8±1.9)ng/L]明显高于野生组[(8.3±1.7)ng/L](P<0.05)。突变组治疗48周后获得完全应答率[46.9%(23/49)]显著高于野生组[16.4%(10/61)]χ^2=7.083,P=0.018;突变组治疗24周后HBsAg下降>1 lg10者较下降≤1 lg10者治疗前的血清Mig显著升高[(129.2±37.9)ng/L与(91.5±25.7)ng/L](P<0.05)。突变组治疗12、24周血清IL-9分别为(8.8±1.9)、(8.9±1.6)ng/L,均较治疗前显著降低(P均<0.05)。结论CHB且HBeAg阳性患者治疗前血清IL-9的高表达与HBV前C/BCP区的变异关系密切,IL-9的表达与干扰素抗病毒疗效无相关性;患者治疗前Mig的高表达可能对HBV前C/BCP区变异者干扰素抗病毒疗效更有利。
