慢性乙型肝炎患者血清sCD14变化意义的初步探讨

目的阐明可溶性CD14(sCD14)在慢性乙型肝炎(慢乙肝)肠源性内毒素血症中的作用.方法ELISA双抗体夹心法测定了60例慢乙肝患者血清sCD14和TNF-α水平,应用基质显色法鲎试验定量检测血浆内毒素水平.结果慢乙肝(轻度)患者血清sCDl4水平与对照组无显著差异外,慢乙肝(中度和重度)sCD14水平均显著高于对照组;慢乙肝伴肠源性内毒素血症时sCD14s为(4.8±2.3)μg/ml,而不伴肠源性内毒素血症者的sCD14为(2.9±1.9)μg/ml,两者之间有显著差异(P＜0.01).慢乙肝(轻度)sCD14水平为(3.0±1.7)μg/ml,TNF-α为(4.69±2.75)ng/ml,两者之间无显著相关(r=0.26,P＞0.05),而慢乙肝(中度和重度)的sCD14水平分别为(5.2±2.1)μg/ml和(6.9±3.4)μg/ml,TNF-α分别为(9.48±6.15)ng/ml和(14.23±8.29)ng/ml,慢乙肝(中度和重度)的sCD14水平分别与其TNF-α有显著相关(r=0.87,P＜0.01;r=0.91,P＜0.01).结论血清中sCD14水平影响并调节内毒素对肝细胞的毒性,临床测定肝病患者sCD14水平,有助于阐明慢性肝病时肠源性内毒素血症在继发性肝损害中的作用.     

酒精性肝病的内毒素及细胞因子改变

酒精性肝病(ALD)的发病机制中,内毒素血症,枯否细胞激活,细胞因子网络改变起重要作用,现综述如下。 1.酒精与内毒素血症:在正常情况下,可有少量的内毒素通过肠壁渗透,进入肝脏。与内毒素结合蛋白(LPB)结合,然后由枯否细胞清除。有证据表明,嗜酒者血液内毒素水平升高。因酒精可改变肠道菌丛,引起G-细菌过度生长,酒精使     

Association of Salivary sCD14 Concentration Levels with Early Childhood Caries

Background: Early childhood caries (ECC) is a severe type of dental caries affecting infants and pre-school children. Because of the infectious nature of the disease, the immunologic response by the host plays an essential role in its development. Objective: This study investigated the association between the presence of salivary sCD14 and ECC. Methods: This study was carried out on 40 healthy children, of whom 20 were caries-free (CF) and 20 had ECC, within the ages of 36 to 71 months. Unstimulated saliva of the children was collected with disposable needle-less syringe from buccal and labial vestibules. Seven children with ECC received complete treatments. Saliva was collected for a second time after 3 months from this group. The sCD14 levels in salivary samples were analyzed by ELISA method. Results: Mean concentrations of sCD14 in ECC and CF groups were 57.82 and 31.92 ng/ml respectively (p=0.008). After three months, the mean concentration of sCD14 among the treated children decreased to 11.38 ng/ml, which was significantly lower compared to that of ECC children before intervention (p<0.001), and also CF children (p<0.05). Conclusion: The increased levels of sCD14 can be considered as a marker of inflammation and innate immune response during ECC.     

内毒素及其结合因子与酒精性肝病的相关性

目的　探讨内毒素及其结合因子与酒精性肝病 (ALD)发生、发展的关系。方法　选取 3 0例ALD患者和 3 0例健康体检者分别作为ALD组与对照组 ,ALD组按临床体征、肝功能和(或 )肝脏B超、病理分为轻、中、重型。均分别检测丙氨酸氨基转移酶 (ALT)、天冬氨酸氨基转移酶(AST)、总胆红素 (TBIL)、内毒素、脂多糖结合蛋白 (LBP)、sCD14、载脂蛋白A1 、A2 、B (ApoA1、ApoA2、ApoB)等指标。 结果　ALD组的ALT、AST、TBIL、内毒素、LBP、sCD14与对照组比较均显著升高 (P <0 .0 5 ) ,且轻、中型ALD患者内毒素、sCD14增加非常显著 (P <0 .0 1) ;轻、中型ALD患者ApoA1、ApoA2显著升高 (P <0 .0 5 ) ,重型患者则减少 ;ApoB在各组患者中变化不明显。内毒素与LBP和sCD14显著相关 (P <0 .0 5 )。结论　内毒素及其结合因子在不同程度的酒精性肝病中的表达有差异 ,提示它们在酒精性肝病的发生、发展中起一定的作用     

脓毒症患者血清中TLR-4、TREM-1、sCD14和IL-18的变化

目的探讨脓毒症患者血清TLR-4、TREM-1、sCD14和IL-18含量的变化与脓毒症严重程度的相关性及用于诊断脓毒症的敏感度与特异度。方法选取60例脓毒症患者及30例正常体检者,分别抽血采用酶联免疫法(ELISA法)测TLR-4、TREM-1、sCD14和IL-18的含量。脓毒症患者根据当天进行APACHE-Ⅱ评分结果,按评分≥20分和20分进入高评分及低评分脓毒症组。结果脓毒症患者上述各因子的含量治疗前均明显高于治疗后,并高于正常对照组(p值均0.05),并且与APACHE-Ⅱ评分呈正相关(r=0.651、0.662、0.652、0.668,P均0.05)。治疗前高评分脓毒症组血清中TLR-4、TREM-1、sCD14、IL-18的含量均明显高于低评分脓毒症组(P均0.05);脓毒症患者治疗前血清中上述细胞因子的ROC曲线下面积分别为1.000、0.795、0.828、0.834及0.850,APACHE-Ⅱ、TLR4、TREM-1及sCD-14分别取20、25.8 ng/ml、89.6 ng/ml及75 ng/ml为截断点,评价预后敏感性分别为为99%、82%、82%及91%,特异性分别为为100%、52%、66%及72%。结论脓毒症患者血清中TLR-4、TREM-1、sCD14、IL-18的含量与脓毒症的发生发展关系密切;通过监测上述细胞因子的含量可以对脓毒症病情严重程度做出一定的判断;TREM-1有可能成为诊断脓毒症较好的实验室指标之一,sCDl4有望成为较为敏感的脓毒症诊断标志物之一。     

糖耐量异常急性冠状动脉综合征患者血清sCD40L水平与sICAM-1的相关性分析

目的:探讨急性冠状动脉(冠脉)综合征患者在小同糖耐量状态下,血清sCD40L水平与sICAM-1 变化的相关性.方法:入选急性冠脉综合征患者148例,根据OGTT试验结果分为3组:糖耐量正常组、糖耐量减低组和糖尿病组,3组均于入院时即行酶联免疫吸附测定法(ELISA)检测血清sCD40L和sICAM-1的水平.结果:3...     

酒精性肝病患者血清细胞因子水平和肠道菌群分布变化研究*

目的 调查酒精性肝病（ALD）患者血清细胞因子水平和肠道菌群分布变化情况。方法 本研究纳入34例ALD患者和34例健康人,采用ELISA法检测血清肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和核因子κB （NF-κB）水平,采用Celsis ^® Advance II^TM快速微生物检测系统检测肠道菌落数。结果 ALD患者空腹血糖（FBG）、总胆固醇（TC）、三酰甘油（TG）、低密度脂蛋白（LDL-C）和高密度脂蛋白（HDL-C）水平分别为（5.3±1.8）mmol/L、（2.3±0.9） mmol/L、（5.1±1.8） mmol/L、（2.1±0.6） mmol/L和（0.9±0.2） mmol/L,与健康人的（5.2±1.3）mmol/L、（2.2±1.1） mmol/L、（5.1±1.6） mmol/L、（2.0±1.5） mmol/L和（0.8±0.1） mmol/L比,差异无统计学意义（P>0.05）;ALD患者血清谷丙转氨酶（ALT）、谷草转氨酶（AST）、谷氨酰转肽酶（GGT）和总胆红素（TBIL）水平分别为（99.5±41.8） U/L、（106.9±55.7） U/L、（229.4±148.3） U/L和（35.3±8.6） μmol/L,显著高于健康人【分别为（35.6±9.7）U/L、（36.2±8.4） U/L、（46.7±14.5） U/L和（16.4±2.3） μmol/L,P<0.05】;ALD患者血清TNF-α、IL-6和N F-κB 水平分别为（9.8±3.4） ng/L、（0.9±0.4） pg/mL和（3.7±6.3） ng/L,显著高于健康人【分别为（5.7±2.1） ng/L、（0.5±0.3） pg/mL和（0.5±0.4） ng/L,P<0.05】;ALD患者粪便粪肠球菌和大肠埃希菌数分别为【（8.7±1.4） lg CFU/g和（7.6±1.2）lg CFU/g】,显著高于健康人【分别为（7.2±1.3） lg CFU/g和（6.6±1.5） lg CFU/g,P<0.05】,而双歧杆菌数为（7.1±1.2）lg CFU/g,显著低于健康人【（8.9±1.3） lg CFU/g,P<0.05】。结论 相对于健康人群,ALD患者存在肠道菌群和血清细胞因子水平紊乱现象,可能参与了疾病的发生发展过程。     

CD14与酒精性肝病

白细胞分化抗原14(clusterofdifferentiationantigen,CD14)为内毒素脂多糖(lipopolysac-charide,LPS)高亲和力受体,在机体免疫、防御系统引起的一系列反应中起着关键的作用.细胞膜CD14识别LPS并引起细胞酪氨酸磷酸化、核因子(nuclearfactor-κB,NF-κB)转位、触发细胞因子释放和氧自由基的产生.而可溶性CD14则与细胞膜CD14竞争结合LPS,并且介导不表达膜CD14的内皮细胞和平滑肌细胞对LPS的应答.近年来发现,CD14在酒精性肝病的发病机制中起着重要的作用.     

sCD163和铁蛋白在HBV相关慢加急性肝功能衰竭中的表达及其临床意义

目的：研究 HBV相关慢加急性肝功能衰竭（HBV-ACLF）患者血浆中可溶性 CD163（sCD163）和铁蛋白水平,分析其与患者病情、预后的关系。方法选择HBV-ACLF患者30例、乙型肝炎肝硬化25例、慢性乙型肝炎18例以及健康对照15例,采用ELISA方法检测血浆中 sCD163和铁蛋白水平。结果 HBV-ACLF 组血浆中 sCD163和铁蛋白水平均明显高于肝硬化组、慢性乙型肝炎组及健康对照组[sCD163：（123±43）比（76±33）、（58±19）、（35±15）ng/mL,均P＜0．05;铁蛋白：（2714±1896）比（505±722）、（833±801）、（106±58）ng/mL,均P＜0．05]。肝衰竭发展到晚期时sCD163和铁蛋白水平均较早、中期明显增高[sCD163：（162±44）比（104±40）、（108±24）ng/mL,均P＜0．05）;铁蛋白：（4154±2122）比（1746±1047）、（2416±1713）ng/mL,均P＜0．05]。HBV-ACLF死亡组中sCD163和铁蛋白水平均高于存活组[sCD163：（140±42）比（101±36）mg/mL,（t＝-2．719,P＝0．01）;铁蛋白：（3568±2007）比（1598±957）ng/mL,（t＝-3．547,P＝0．001）]。经受试者工作特征曲线（ROC）分析,sCD163、铁蛋白评估 HBV-ACLF患者3个月内死亡所对应的曲线下面积（AUC）分别为0．803、0．844。结论 sCD163和铁蛋白可作为 HBV-ACLF病情严重程度及预后评估的重要参考指标。     

CD14 promoter polymorphism in Chinese alcoholic patients with cirrhosis of liver and acute pancreatitis

AIM: To investigate the relationship between genetic polymorphism of the CD14 promoter and the occurrence of alcoholic cirrhosis and alcoholic pancreatitis, and to challenge the conclusion made earlier that the patients with acute alcoholic pancreatitis and patients with alcoholic cirrhosis of liver are two different subpopulations. METHODS: Using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method, we determined the polymorphism of CD14 gene and aldehyde dehydrogenase gene 2 (ALDH 2) in 335 alcoholic patients with different organ complications i.e., cirrhosis of liver (n = 100), acute pancreatitis (n = 100), esophageal cancer (n = 82) and avascular necrosis of hip joint (AVN) (n = 53) and 194 non-alcoholic controls in a Chinese group. RESULTS: The results showed that the carriage of T allele was not different among alcoholic patients with cirrhosis of liver, alcoholic patients with other complication and non-alcoholic controls. On the other hand, the carriage of the C allele was significantly more prevalent for alcoholic pancreatitis than for esophageal cancer (0.79 vs 0.60, P<0.001), alcoholic AVN (0.79 vs 0.65, P<0.025) and nonalcoholic controls (0.79 vs 0.68,P<0.025). Furthermore, when only subjects with ALDH2 1-1 genotype were examined, the C allele frequency was significantly more prevalent for alcoholic pancreatitis than for alcoholic liver cirrhosis (0.82 vs 0.69,P<0.025), esophageal cancer (0.82 vs 0.61,P><0.01), alcoholic AVN (0.82 vs 0.64, P<0.01) and non-alcoholic controls (0.82 vs 0.69, P<0.05). CONCLUSION: The C allele may be associated with some mechanism, which is important in the pathogenesis of alcoholic pancreatitis, and that alcoholic patients with acute pancreatitis and cirrhosis of liver are probably two different subpopulations.     

HCV感染患者免疫细胞部分细胞因子分泌情况的初步研究

目的研究与正常人比较丙型肝炎病毒（HCV）感染患者免疫细胞分泌γ干扰素（IFN-γ）、白细胞介素10（IL-10）、肿瘤坏死因子α（TNF-α）及白细胞介素4（IL-4）的细胞频数情况,了解HCV感染对其影响。方法分离外周血单核细胞（PBMCs）,应用IL-10、IFN-γ、TNF-α及IL-4流式抗体进行细胞内因子染色,应用FACSCalibur流式细胞仪及FACSCalibur软件进行检测分析。结果HCV感染患者分泌IL-10、IFN-γ、IL-4的细胞频数在CD4＋CD8-T细胞、CD4-CD8＋T细胞、NK细胞和NKT细胞均发生明显下降;分泌TNF-α的细胞频数在CD4-CD8＋T淋巴细胞及NK细胞出现下降;HCV感染患者NK细胞、NKT细胞分泌IL-10和IFN-γ的细胞频数较CD4＋CD8-T淋巴细胞、CD4-CD8＋T淋巴细胞下降得更加明显。结论HCV感染患者的细胞免疫功能受到明显的损害,细胞因子分泌能力明显减低;固有免疫细胞功能受损可能是HCV感染慢性化的重要原因;细胞因子分泌的调节是抗HCV感染免疫治疗过程中需要调节的方向。     

Different effects of a CD14 gene polymorphism on disease outcome in patients with alcoholic liver disease and chronic hepatitis C infection

AIM: Clinical and experimental data suggest that gut-derived endotoxins are an important pathogenic factors for progression of chronic liver disease. Recently, a C-T (-159) polymorphism in the promoter region of the CD14 gene was detected and found to confer increased CD14 expression and to be associated with advanced alcoholic liver damage. Here, we investigated this polymorphism in patients with less advanced alcoholic liver disease (ALD) and chronic hepatitis C virus (HCV) infection. METHODS: CD14 genotyping was performed by PCR-RFLP analysis in (a) 121 HCV patients, (b) 62 patients with alcohol-associated cirrhosis (Alc-Ci), (c) 118 individuals with heavy alcohol abuse without evidence of advanced liver damage (Alc-w/o Ci), and (d) 247 healthy controls. Furthermore, serum levels of soluble CD14 (sCD14) and transaminases were determined. RESULTS: The TT genotype was significantly more frequent in Alc-Ci compared to Alc-w/o Ci or controls (40.3% vs 23.7% or 24.0%, respectively). In Alc-w/o Ci, serum levels of transaminases did not differ significantly between patients with different CD14 genotypes. In HCV patients, TT-homozygotes had significantly higher sCD14 levels and sCD14 serum levels were significantly higher in patients with advanced fibrosis or cirrhosis. However, no association was found between CD14 genotypes and histological staging or grading. CONCLUSION: Considering serum transaminases as surrogate markers for alcoholic liver damage, the CD14 polymorphism seems to exhibit different effects during the course of ALD. Differences in genotype distribution between cirrhotic HCV patients and alcoholics and the known functional impact of this polymorphism on CD14 expression levels further indicate differences in the pathophysiological role of CD14 and CD14-mediated lipopolysaccharides signal transduction with regard to the stage as well as the type of the underlying liver disease.     

Serum and bronchial lavage fluid concentrations of IL-8, SLPI, sCD14 and sICAM-1 in patients with COPD and asthma

BACKGROUND: Airway inflammation is associated with an increased expression and release of inflammatory reactants that regulate processes of cell migration, activation and degranulation. The purpose of this study was to quantify bronchial lavage (BAL) fluid and serum levels of chemokine (IL-8), secretory leukocyte protease inhibitor (SLPI), soluble intracellular adhesion molecules-1 (sICAM-1) and sCD14, as surrogate markers of inflammatory and immune response in asthma and chronic obstructive pulmonary disease (COPD) patients with similar disease duration time. METHODS: Biomarkers in serum and BAL fluid from asthma (n=13) and COPD (n=25) patients were measured using commercially available ELISA kits. RESULTS: We found that in asthma and COPD groups the concentrations of IL-8 and SLPI are significantly higher in BAL fluid than in serum, while levels of sICAM-1 and sCD14 in BAL fluid are significantly lower than in serum. Of these 4 measured biomarkers, only the BAL IL-8 was higher in COPD patients when compared to asthma (P<0.05). In both groups, BAL IL-8 correlated with SLPI (r=0.577, P<0.01 and r=0.589, P<0.05, respectively). In patients with COPD the BAL sICAM-1 correlated with sCD14 (r=0.576, P<0.01), while in asthma patients BAL sICAM-1 correlated with FEV(1)/FVC (r=0.418, P<0.01). Moreover, in asthma patients the serum SLPI correlated with sCD14 (r=0.688, P<0.01) and serum sICAM-1 negatively correlated with FEV(1)/FVC (r=-0.582, P<0.05). CONCLUSION: Our findings point to the importance of selecting a correct biological fluid when analyzing specific biomarkers, and also show that of 4 measured biomarkers, only the BAL IL-8 was higher in COPD patients when compared to asthma.     

Serum levels of macrophage migration inhibitory factor, Interleukin-17 and Interleukin-10 in patients with HBV-related liver disease

Objective To study the potential role of macrophage migration inhibitory factor(MIF),Interleukin-17(IL-17) and Interleukin-10(IL-10) in the development of HBV-related liver disease.Methods 48 patients with chronic hepatitis B(HBeAg negative and positive,24 cases;21cases of HBV-DNA negative and 27 cases of HBV-DNA positive),81 cases of hepatitis B patients with decompensated cirrhosis and 48 cases of primary liver cancer patients were collected as the experimental group,26 healthy people were as control group.Serum MIF,IL-17 and IL-10 were measured.Results MIF and IL-17 significantly increased,IL-10 significantly decreased in experimental group,compared with the control group(P<0.05),there was significant difference.In addition,there was no significant difference(P>0.05) between positive and negative of chronic hepatitis B.MIF,IL-17 and ALT levels were positively correlated(r=0.693,P<0.01;r=0.897,P<0.001),IL-10 and ALT was negatively correlated(r =-0.285,P=0.037).Conclusion These results indicated that MIF,IL-17 and IL-10 may participate in the pathological process of HBV-related liver disease,serum levels of MIF,IL-17 and IL-10 appear to reflect the severity of tissue injury in HBV-related liver disease.     

慢性乙型肝炎外周血sCD62E水平与肝功能的关系

采用双抗体夹心ELISA法检测54例慢性乙型肝炎患者外周血可溶性选择素E（sCD62E)浓度变化并分析其与肝功能的关系。结果显示：慢性乙肝患者外周血sCD62E水平明显高于对照组（P＜0．001）。慢乙肝轻度、中度、重度三组sCD62E均显著高于对照组（P＜0．01）。轻为、中度、重度慢乙肝患者sCD62E逐渐升高且差异明显。sCD62E与ALT、AST、TBIL呈正相关，与ALB负相关。提示：sCD62E水平越高，肝功能损害越明显。sCD62E水平对衡量肝脏炎症程度和判断预后有重要临床价值。CD62E在HBV感染后引起的淋巴细胞浸润及肝细胞损伤机理中可能有重要作用。     

阿奇霉素对COPD稳定期患者血清IL-4及IL-10的影响

目的观察阿奇霉素治疗COPD稳定期患者外周血IL-4、IL-10指标的变化。方法选择我院门诊COPD稳定期患者108例,随机分为实验组和对照组(每组54例)。对照组给予常规治疗,实验组在常规治疗上加口服阿奇霉素。两组在治疗前及治疗后3月、6月、9月检测血清IL-4、IL-10水平变化。结果两组患者血清IL-4、IL-10水平在治疗前及治疗后3个月差别无统计学差异(P0.05)。实验组血清IL-4及IL-10在治疗后6月、9月水平均明显高于对照组(P0.05)。结论阿奇霉素具有免疫调节功能,可增加抗炎因子,口服方便、安全、有效,在治疗COPD患者中具有一定临床应用价值。     

血清内毒素结合蛋白和sCD163水平预测亚急性肝衰竭患者预后的价值分析

目的 探讨应用血清内毒素结合蛋白(LBP)和可溶性CD163(sCD163)预测亚急性肝衰竭(SALF)患者预后的价值.方法 2019年1月～2020年1月在我院接受治疗的60例SALF患者和同期在我院接受体检50例健康人,采用ELISA法检测血清LBP和sCD163.记录死亡例数,获得终末期肝病模型评分(MELD)....     

The levels of sCD30 and of sCD40L in a group of patients with systemic lupus erythematodes and their diagnostic value

CD30/CD30L and CD40/CD40L are molecules from the tumor necrosis factor (TNF) superfamily. They have a major effect on communications between the B and T cells, which leads to control of maturation, proliferation, and apoptosis of those cells. The aim of this study was to compare the levels of a soluble form of CD30 (sCD30) and a soluble ligand CD40 (sCD40L) in patients with systemic lupus erythematosus (SLE) (n=65) and healthy controls (sCD30 n=20, sCD40L n=10) with other parameters of SLE activity. Patients were divided into subgroups according to presence or absence of lupus nephritis (LN; 33 with LN, 32 without LN). The serum levels of selected parameters were assessed also in the subgroups with low active disease characterized by European Lupus Activity Measure (ECLAM) at most 3(n=29) and active disease with ECLAM more than 3 (n=36). The serum levels of sCD30 were 66.0±40.2 UI/ml in the whole group. The mean serum levels were 60.0±45.2 UI/ml in the subgroups with LN, 67.1±38.9 UI/ml in the subgroup without LN, 80.2±51.9 UI/ml in the subgroup with active disease, 55.4±24.1 UI/ml in the subgroup with low active disease, and finally, 40.1±19.2 U/ml in the controls. Significant differences were found between the SLE patients and controls (p=0.0001) and between the active and nonactive groups (p=0.002). A correlation was found between levels of CD30 and ECLAM (r=0.25, p≤0.05), SLEDAI (SLE Disease Activity Index) (r=0.25, p≤0.05), C4 component of the complement system (r=0.24, p=0.02), and anti-C1q antibodies (r=0.42, p=0.0001). The levels of sCD40L were 7.4±6.7 ng/ml in whole SLE group, 7.0±8.1 ng/ml in the subgroup with LN, 8.0±4.9 ng/ml in the subgroup without LN, 7.1±5.0 ng/ml in the group of patients with active disease, 7.73±7.8 ng/ml in the subgroup with low activity, and 2.96±1.39.0 ng/ml in the controls. The difference in sCD40L serum levels between patients with SLE and controls was statistically significant (p=0.02). A correlation was found with the anti-C1q antibodies (r=0.21, p=0.05); no other correlations were found. These findings indicate some potentional role of both serum parameters in measurement or SLE disease activity, although their usage in the diagnostic of disease requires further investigation.