重型乙型肝炎肝内细胞间粘附分子—1 mRNA的表达

目的 探讨细胞间粘附分子－１（ＩＣＡＭ－１）ｍＲＮＡ在重型乙型肝炎肝内的表达水平及其意义。方法 用原位杂交技术检测１１例非肝病对照者,５例慢性无症状ＨＢｓＡｇ携带者（ＡｓＣ）,１５例慢性乙型肝炎和３０例重型乙型肝炎患者肝内ＩＣＡＭ－１ ｍＲＮＡ原位表达。结果 非肝病者和ＡｓＣ肝细胞无ＩＣＡＭ－１ ｍＲＮＡ;重型乙型肝炎患者肝细胞ＩＣＡＭ－１ ｍＲＮＡ表达明显增强,其表达水平显著高于慢性乙型肝炎。结     

慢性乙型病毒性肝炎患者血清可溶性细胞间粘附分子-1作用的初步探讨

探讨可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）在慢性乙型肝炎中的作用及临床意义。应用酶联免疫吸附试验检测５６例慢性乙型肝炎患者血清ｓＩＣＡＭ－１水平。慢性乙型肝炎患者血清ｓＩＣＡＭ－１水平明显高于正常人水平，且随着肝细胞损伤程度的加重而升高于正常人与Ｔ细胞亚群无相关性。血清ｓＩＣＡＭ－１水平可反映慢性乙型肝炎患者的病情及肝细胞坏死程度，不能直接影响其细胞免疫功能。     

细胞间粘附分子－1在乙型肝炎中的表达及意义

为观察细胞间粘附分子－１（ＩＣＡＭ－１）在乙型肝炎肝组织内的表达状况，探讨ＩＣＡＭ－１在乙型肝炎肝细胞免疫损伤中的作用。采用链菌素亲生物蛋白法（ＬＳＡＢ），以ＩＣＡＭ－１的单克隆抗体，检测１０４例急、慢性乙型肝炎，９例无症状携带者，１０例正常肝组织标本内ＩＣＡＭ－１抗原表达情况。结果发现：ＩＣＡＭ－１在正常肝细胞无表达，肝窦内皮细胞弱表达；ＨＢＶ感染后肝细胞呈不同程度的表达，肝窦内皮表达增强；中、重度慢性肝炎，活动性肝硬化肝细胞ＩＣＡＭ－１表达较急性肝炎，轻度慢性肝炎显著增强（Ｐ＜０．０１）；急性肝炎较轻度慢性肝炎显著增强（Ｐ＜０．０１）；轻度慢性肝炎较无症状携带者，正常肝组织显著增强（Ｐ＜０．０１）。表明ＩＣＡＭ－１在乙型肝炎肝细胞内表达与肝细胞损伤有关，对ＨＢＶ的清除可能起着重要作用，ＩＣＡＭ－１在肝窦内皮的表达有助于淋巴细胞向肝组织内浸润。     

细胞间黏附分子—1／淋巴细胞功能相关抗原—1在乙型肝炎？…

目的 探讨细胞间黏附分子－１／淋细胞功能相关抗原－１（ＩＣＡＭ－１／ＬＦＡ－１）在乙型肝炎发病机制中的作用。方法 用免疫组化检测１１例正常人和７０例ＨＢＶ感染者肝内ＩＣＡＭ－１、ＬＦＡ－１和ＣＤ８表达状况，并用免疫组化双重染色技术研究ＨＢＶ感染者肝内ＩＣＡＭ－１与ＬＦＡ－１双重表达状况。结果 在炎症坏死区，ＬＦＡ－１阳性淋巴浸润在ＩＣＡＭ－１阳性肝细胞周围，部分与ＩＣＡＭ－１阳性肝细胞紧密接触，Ｌ     

慢性乙型肝炎患者肝组织ICAM-1的表达及与血清sICAM-1水平的关系

目的:探讨慢性乙型肝炎患者肝组织ICAM-1的表达及与血清SICAM-1水平的关系。方法:用免疫组织化学技术及酶联免疫吸附试验检测60例慢性乙型肝炎患者肝组织ICAM-1的表达及血清sICAM-1的水平。结果:慢性乙型肝炎患者肝损害越重、组织坏死越明显,肝细胞ICAM-1表达越强;血清sICAM-1水平,在慢性重型肝炎患者中最高、慢性轻度肝炎患者最低。结论:ICAM-1在乙型肝炎的发病机制中起重要作用,肝组织ICAM-1表达及血清sICAM-1水平,可反映肝组织炎症活动程度及肝细胞坏死程度。     

细胞间粘附分子—1在乙型肝炎中的表达及意义

为观察细胞间粘附分子－１在乙型肝炎肝组织内的表达状况，探讨ＩＣＡＭ－１在乙型肝炎肝细胞免疫损伤中的作用。     

肝癌组织及血清中细胞间粘附分子-1表达的研究

目的研究细胞间粘附分子－１（ｉｎｔｅｒｃｅｌｕｌａｒａｄｈｅｓｉｏｎｍｏｌｅｃｕｌｅ－１，ＩＣＡＭ－１）作为判断肝癌发展程度及转移状态指标的可能性。方法以免疫组化的方法检测ＩＣＡＭ－１在肝癌组织和正常肝组织中的表达，观察了ＩＣＡＭ－１表达在细胞的定位。以点免疫印迹法测定不同患者血清和不同肝组织中ＩＣＡＭ－１的表达。分析ＩＣＡＭ－１表达与肿瘤生长转移状态、肿瘤特性的关系。结果肝癌细胞ＩＣＡＭ－１表达阳性（阳性率为８００％），主要分布在细胞膜，正常肝细胞则为阴性。肝癌患者血清可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）水平高于正常人（Ｐ＜００１）及肝良性肿瘤患者（Ｐ＜００５），肝癌伴转移者高于无转移者（Ｐ＜００５）。肝癌组织中ＩＣＡＭ－１含量明显高于癌旁组织（Ｐ＜００１）及正常肝组织（Ｐ＜００１），而与肿瘤大小及有无包膜无关（Ｐ＞００５）；转移组肝癌中ＩＣＡＭ－１的表达明显高于非转移组（Ｐ＜００５），两组癌旁组织中ＩＣＡＭ－１表达无差别（Ｐ＞００５）。结论血清及组织中ＩＣＡＭ－１的水平在一定程度上可以反映肝癌发展程度及转移状态，有可能作为预测肝癌转移复发的指标。     

可溶性细胞间粘附分子—1在慢性乙型肝炎的临床意义

观察慢性乙型肝炎患者血清可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）的变化，探讨其临床意义及在发病机制中的作用。方法采用酶联免疫吸附试验（ＥＬＩＳＡ）法测定５６例慢性乙肝患者（其中 慢性轻度２０例，中度２４例，重度６例，慢性重型６例）血清ｓＩＣＡＭ－１水平，同时检测血清肿瘤坏死因子－α，肝功能，并以２０例健康人员作对照。结果（１）慢性乙肝患者血清ｓＩＣＡＭ－１水平（轻度６８２．５６２６７．３９ｎｇ     

重型乙型病毒性肝炎肝内ICAM-1 mRNA表达

目的探讨细胞间粘附分子-1(ICAM-1)mRNA在重型乙型肝炎肝内的表达水平及其意义。方法用原位杂交技术检测11例正常人,5例慢性无症状HBsAg携带者(AsC)、15例慢性乙型肝炎和30例重型乙型肝炎患者肝内ICAM-1 mRNA原位表达。结果正常人和AsC肝细胞无ICAM-1 mRNA表达;重型乙型肝炎患者肝细胞ICAM-1 mRNA表达明显增强,其表达水平显著高于慢性乙型肝炎。结论ICAM-1在重型乙型肝炎肝坏死中起重要作用。     

慢性肝病患者血清可溶性细胞间粘附分子—1和有质酸水平的变？…

目的：探讨血清可溶性细胞间粘附分子－１（ｓＩＣＡＭ－１）秀有质酸（ＨＡ）与肝纤维化及肝损害的关系。方法：用ＥＬＩＳＡ法检测正常人、慢性肝炎肝硬变患者血清ｓＩＣＡＭ－１;用ＲＩＡ法测定正常人、慢性肝炎及肝硬变患者血清ＨＡ。结果：慢性肝病患者且血清ｓＩＣＡＭ－１均显著高于正常人,各组间存在显著的差异。血清ＨＡ水平在慢性肝炎中度组、重度组、肝硬变组明显高于正常人。在不同临床类型的慢性现患者中ＨＡ血清水平     

慢性乙型肝炎肝组织ICAM-1 mRNA和ICAM-1表达及意义

目的探讨肝组织间粘附分子-1(ICAM-1)表达在慢性乙型肝炎(CHB)发病机理中的作用。方法用原位杂交和免疫组织化学技术检测11例正常人和50例慢性HBV感染者肝内ICAM-1 mRNA和ICAM-1表达情况。结果正常人和慢性无症状HBsAg携带者肝细胞无ICAM-1mRNA和ICAM-1表达,CHB患者肝细胞ICAM-1 mRNA和ICAM-1表达增强,阳性肝细胞多分布在汇管区周围和腺泡内炎症坏死区域;重度CHB患者肝细胞ICAM-1 mRNA和ICAM-1表达显著强于中、轻度CHB患者(P<0.05);肝细胞ICAM-1表达强度与肝组织炎症活动度呈显著正相关,p<0.01;肝细胞ICAM-1表达强的患者肝功能显著差于ICAM-1表达弱者,P<0.05。结论肝细胞ICAM-1表达在慢性乙型肝炎肝细胞坏死中起重要作用,肝细胞ICAM-1表达水平能较好反映其肝损害程度和肝功能状况。     

细胞间黏附分子-1/淋巴细胞功能相关抗原-1在乙型肝炎发病机制中的作用

目的　探讨细胞间黏附分子 1/淋巴细胞功能相关抗原 1(ICAM 1/LFA 1)在乙型肝炎发病机制中的作用。方法　用免疫组化检测 11例正常人和 70例HBV感染者肝内ICAM 1、LFA 1和CD8表达状况 ,并用免疫组化双重染色技术研究HBV感染者肝内ICAM 1与LFA 1双重表达状况。结果　在炎症坏死区 ,LFA 1阳性淋巴细胞浸润在ICAM 1阳性肝细胞周围 ,部分与ICAM 1阳性肝细胞紧密接触 ,LFA 1阳性淋巴细胞周围存在坏死细胞碎片和损伤的肝细胞。结论　ICAM 1/LFA 1参与介导淋巴细胞与肝细胞间黏附 ,在慢性乙型肝炎和重型乙型肝炎免疫发病机制中起重要作用。     

乙型肝炎肝组织细胞粘附分子-1表达的免疫组化研究

目的 探讨细胞粘附分子-1(ICAM-1)在乙型肝炎肝组织内的表达与肝细胞损伤的关系。 方法 用免疫组织化学技术,标记的链菌素亲生物蛋白法检测113例急、慢性乙型肝炎,10例正常肝组织标本内ICAM-1抗原表达情况。 结果 中、重度CAH、活动性肝硬变肝细胞ICAM-1表达较急性肝炎、轻度CAH显著增强(P<0.01);急性肝炎、轻度CAH较CPH、ASC、正常肝组织显著增强(P<0.01)。HBV低复制组(HBeAg-,HBeAb )中,肝细胞表达ICAM-1阳性率(92.7％),高于HBeAg ,HBeAb-组(75.7％,P<0.05)。 结论 ICAM-1肝细胞膜表达与乙型肝炎肝细胞损伤有关,在HBV清除过程中可能起着重要作用。     

Intercellular adhesion molecule-1 expression on the hepatocyte membrane of patients with chronic hepatitis B and C

ABSTRACT— The expression of intercellular adhesion molecule-1 (ICAM-1) on the hepatocyte membrane was studied in 27 patients with chronic hepatitis B and C (CHB, CHC) by immunostaining using a monoclonal antibody. ICAM-1 was expressed focally in a honeycomb-like pattern by hepatocytes in livers of 26/27 patients. The degree of ICAM-1 expression was closely related to the ALT level and the histological grade of liver damage. Abundant cytotoxic T cells (CD8 +, CD11b –) were found in ICAM-1-positive areas of the liver. Zones of focal necrosis contained both ICAM-1-positive hepatocytes and cytotoxic T cells. The expression of ICAM-1 was decreased in 4/6 CHB patients after interferon-α therapy. No relationship between the degree of hepatocyte ICAM-1 expression and viral replication markers (DNA polymerase activity and the presence of HBcAg in the liver) was observed in patients with CHB. In addition, no positive correlation was found between the distribution of ICAM-1-positive hepatocytes and HBcAg-positive hepatocytes. These results suggest that ICAM-1 may play an important role in the pathogenesis of hepatocellular injury mediated by cytotoxic T cells in CHB and CHC.     

Immunohistochemical study of the distribution of intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1 in chronic type B hepatitis

The expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) in the livers of 11 patients with chronic hepatitis B was studied immunohistochemically by light and electron microscopy to clarify the role of these adhesion molecules in tissue damage in chronic hepatitis B. On hepatocytes, ICAM-1 expression was confined to the bile canalicular surface when the liver inflammation was mild. In contrast, when the liver inflammation was severe, ICAM-1 was distributed on the entire surface of the hepatocyte, including the sinusoidal and lateral membranes; lymphocytes which were mostly positive for LFA-1, were often observed invading deeply among these hepatocytes. The degree of ICAM-1 expression on the hepatocytes was also related to the expression of HLA class 1 antigen. In liver showing diffuse expression of ICAM-1 on the hepatocytes, strong expression of HLA class 1 antigen was observed, and amounts of HBV in the liver were decreased. Diffuse expression of ICAM-1 and HLA class 1 antigen was mostly observed after acute exacerbation of liver inflammation. These results suggest that the ICAM-1/LFA-1 pathway is involved in the immunological mechanism, responsible for liver cell damage in chronic hepatitis B.     

Hepatocyte membrane-bound IgG and circulating liver-specific autoantibodies in chronic liver disease: relation to hepatitis B virus serum markers and liver histology

Hepatocytes isolated from 101 biopsies were examined for membrane-bound IgG. The sera of the patients were tested for anti-liver-specific lipoprotein by radioimmunoassay and for liver membrane autoantibody (by indirect immunofluorescence on isolated rabbit hepatocytes. The seven patients with normal liver or minor nonspecific alterations were negative for membrane IgG and serum antibodies. Membrane IgG with granular distribution was found in 41 patients [21 hepatitis B virus-related chronic active hepatitis (CAH), 3 cryptogenic CAH, 3 chronic persistent hepatitis, 6 prolonged viral hepatitis, 1 alcoholic cirrhosis, and 6 primary biliary cirrhosis]. Membrane IgG with linear fluorescence pattern was detected in 12 cases (4 autoimmune CAH, 3 HBsAg-positive CAH, 2 alcoholic cirrhosis, 1 anti-HBc positive CAH, 1 cryptogenic CAH, and 1 prolonged viral hepatitis). A strong association between granular IgG and serum HBsAg was found. Nuclear localization of IgG was found in 34 patients and correlated with the positivity of granular membrane IgG. The highest prevalence of anti-liver-specific lipoprotein was found in primary biliary cirrhosis and autoimmune CAH cases which were also positive for liver membrane autoantibody. No relationship was found between the presence of membrane IgG and circulating liver-specific autoantibodies. Membrane IgG and anti-liver-specific lipoprotein correlated with the presence of moderate and severe portal inflammatory infiltration but not with piecemeal necrosis or transaminase levels. Eleven of the twelve patients with linear membrane IgG presented chronic active liver disease with moderate to severe signs of liver damage. Therefore, it is suggested that, while granular membrane IgGs are related to hepatitis B virus, antigenic expression on the hepatocyte surface and/or the presence of immune complexes, linear membrane IgG could play a role in the immunopathogenesis of liver cell damage particularly in "autoimmune" cases which present high percentages of positive cells liver-specific autoantibodies.     

A study of the relation of the expression of beta-microglobulin and hepatocytic lesions in hepatitis B

Beta 2-Microglobulin expression on hepatocyte membrane was studied in 117 liver biopsies from patients with acute and chronic hepatitis B and in 11 subjects with normal liver function, using immunohistochemical PAP method. In normal liver beta 2-microglobulin could not be detected on hepatocyte membrane, compared with that in subjects with normal liver, in asymptomatic HBsAg carrier and in patients with chronic persistent hepatitis, there is significant enhancement of beta 2-microglobulin expression in patients with acute mild hepatitis and chronic mild active hepatitis. Beta 2-Microglobulin expression in patients with chronic active hepatitis with moderate to severe activity and cirrhosis has a significant enhancement, when compared with acute mild hepatitis and chronic mild active hepatitis. Moreover, location of beta 2-microglobulin expression on hepatocyte membrane was associated with lesion of hepatocytes. Enhanced expression of beta 2-microglobulin on hepatocyte membrane in acute and chronic hepatitis B probably reflects enhanced display of HLA-ABC antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of T cell-mediated hepatocytelysis.