PECAM-1在炎症微循环损伤中的作用

炎症过程的一个重要特征是白细胞粘附并穿越微血管内皮细胞,向炎症部位募集.外渗的白细胞释放细胞毒性物质,如氧自由基、蛋白水解酶等,造成组织损伤.在炎症反应中,白细胞与内皮细胞的相互作用是一重要环节,它决定了白细胞经内皮迁移以及粘附分子参与白细胞粘附的整个过程.在炎症所致微循环损伤中,血小板内皮细胞粘附分子 - 1( PECAM- 1, CD31) 扮演了重要角色.     

支气管哮喘患者外周血中sICAM—1的水平与嗜酸性细胞的激活

支气管哮喘患者外周血中ｓＩＣＡＭ１的水平与嗜酸性细胞的激活谢华孙滨（第四军医大学西京医院呼吸科，西安７１００３２）嗜酸性细胞在哮喘炎症中起着重要的作用，其募集到炎症部位前，须先和血管内皮细胞粘附。其中血管内皮细胞上的血管细胞粘附分子１（ＶＣＡＭ?..     

粘附分子与疾病

粘附分子(Adhesion Molecnles)是一类能介导细胞间粘附以及细胞与细胞外基质粘附的糖蛋白。随着粘附分子的不断深入研究,目前已发现了多种粘附分子,通过阐明粘附分子与疾病的关系,可为临床应用打下基础。本文主要概述以下两个方面:1.几种主要与炎症有关的粘附分子,如:LFA-1,ICAM-1,VLA-4,CD44。2.粘附分子与几种疾病的关系。如:白细胞粘附不全症、类风湿性关节炎、获得性免疫缺陷综合征以及支气管哮喘。     

血清sICAM-1和sVCAM-1在支气管哮喘发病中的意义

细胞间粘附分子 1(ＩＣＡＭ 1)和血管内皮细胞粘附分子 1(ＶＣＡＭ 1)均属于免疫球蛋白超家族中的成员。许多研究已证实ＩＣＡＭ 1、ＶＣＡＭ 1与嗜酸性粒细胞在变态反应炎症部位的移行和募集有关。有人在哮喘实验的动物模型中采用免疫组化法 ,发现在气道粘膜下ＩＣＡＭ 1〔1〕和ＶＣＡＭ 1表达增加〔2〕。参与免疫反应的粘附分子可从表达的内皮细胞或激活的淋巴细胞上脱落下来 ,进入血液成为可溶性粘附分子 ,从而发生一系列免疫反应。本研究试图通过血清中可溶性粘附分子 (ｓＩＣＡＭ 1和ｓＶＣＡＭ 1)含量的变化 ,分析其是否与支气管哮喘…     

白细胞介素17在大鼠哮喘模型肺组织的表达及意义

白细胞介素17(IL-17)是由激活的T淋巴细胞产生的细胞因子，研究证实该细胞因子能增强气道上皮细胞内细胞间粘附分子1(ICAM-1)表达。支气管哮喘不仅气道粘膜存在大量T淋巴细胞浸润，气道内炎性细胞包括中性粒细胞及嗜酸细胞聚集也增多，而ICAM-1在炎性细胞气道聚集中发挥重要作用。     

粘附分子与哮喘气道炎症细胞的迁移

近年研究提出，粘附分子作为前炎症物质在支气管哮喘发病中起重要的作用，本文就粘附分子在哮喘气道炎症细胞的迁移，特别是选择性地介导嗜酸性，嗜碱性粒细胞和Ｔ细胞跨内皮迁移，以及粘附分子在哮喘中的研究进展做一综述。     

支气管哮喘患者血浆sICAM-1、嗜碱性细胞及嗜酸性细胞的变化及其意义

支气管哮喘是一种以气道高反应性为特点的慢性气道变应性炎症, 此种炎症与T淋巴细胞、嗜碱性细胞及嗜酸性细胞浸润、激活及所释放的细胞因子和介质有关. 近年来研究表明, 这些细胞在血管内流动, 粘附于内皮细胞, 并激活穿过内皮细胞进入气道粘膜层, 与多种趋化因子和粘附分子有关[1].本文着重探讨粘附分子中的重要成份可溶性细胞间粘附分子-1(sICAM-1)在哮喘中的变化以及与嗜碱性细胞和嗜酸性细胞的关系.     

细胞间粘附分子-1 RIA的临床应用

粘附分子是一类介导细胞与细胞、细胞与细胞外基?质间粘附作用的膜表面糖蛋白.它们在胚胎发育和分化、正常组织结构的维持、炎症与免疫应答、伤口修复、凝血及肿瘤的进展与转移等多种生理病理过程中均具有重要作用[1].细胞间粘附分子-1(ICAM-1)属于粘附分子免疫球蛋白超家族的成员,目前对于ICAM-1与疾病的关系报告较多.本文仅就ICAM-1在肝细胞性肝癌(HCC)、病毒性肝炎(VH)、糖尿病(DM)、多发性硬化症(MS)等疾病中的含量变化及临床研究文献资料作一简要概述.     

哮喘青春期缓解者外周血可溶性血管细胞粘附分子-1的测定

血管细胞粘附分子 1(ＶＣＡＭ 1)主要表达于活化的内皮细胞 ,它介导了炎症细胞与血管内皮细胞的粘附和跨内皮转移 ,在气道粘膜的嗜酸粒细胞 ,淋巴细胞的选择性聚集、浸润中起重要作用[1] 。可溶性血管细胞粘附分子 1(ｓＶ ＣＡＭ 1)是存在于血清中的从血管内皮细胞上自然脱落的ＶＣＡＭ 1分子 ,是反映体内ＶＣＡＭ 1表达水平的可溶性标志物。临床上某些哮喘儿童到青春期会自然缓解甚至痊愈是个普遍现象[2 ] ,其机制尚未阐明。本实验通过对哮喘青春期缓解组、哮喘组和正常对照组的外周血ｓＶＣＡＭ 1水平的测定和比较 ,探索其中的规律。1　…     

细胞间粘附分子-1在血脑屏障上的表达和调控

血脑屏障(BBB)主要由脑微血管内皮细胞(BMEC)相互紧密连接而成，可阻止物质进入中枢神经系统(CNS)。CNS要保持稳定独特的微环境有赖于BBB结构的完整。在多发性硬化(MS)等神经系统自身免疫性疾病中，由于BBB遭到破坏，血管周围细胞(星形细胞、巨噬细胞和小胶质细胞)及脑微血管内皮细胞(BMEC)释放多种炎性因子，脑和脊髓毛细血管内皮细胞上的粘附分子(AMs)的表达发生改变，从而影响BBB的通透性。其中细胞间粘附分子-1(ICAM-1)可与白细胞上的配体结合，使白细胞活化后进入CNS。本文就ICAM-1表达和调控与BBB相关的几个问题作一综述。     

Elevated levels of soluble ICAM-1 in sera from patients with bronchial asthma

We measured the levels of soluble intercellular adhesion molecule-1 (sICAM-1) in sera from patients with bronchial asthma. sICAM-1 levels in sera from atopic asthmatic patients in stable conditions were higher than in normal control subjects. Furthermore, the sICAM-1 levels in sera obtained during bronchial asthma attacks were higher than those in sera obtained in stable conditions. These results suggest that higher levels of sICAM-1 in sera reflect the upregulation of ICAM-1 expression in allergic inflammation.     

Circulating soluble intercellular adhesion molecule-1 (sICAM-1) in patients with sarcoidosis

sICAM-1 has been elevated in sera of specific inflammatory diseases, and circulating sICAM-1 concentrations reflect disease activity in these diseases. We measured circulating sICAM-1 concentrations and serum angiotensin-converting enzyme (SACE) activity in patients with sarcoidosis. Patients with sarcoidosis had significantly increased circulating sICAM-1 concentrations (62.8±33.5U/ml) and SACE activity (23.7±7.4U/l) compared with controls (circulating sICAM-1 50.9±12.1U/ml, and SACE 13.5±3.8U/l). Successive measurements showed that circulating sICAM-1 values changed in parallel with disease activity in sarcoidosis. In the progressive disease group (progressed or without change for 2 years or more), circulating sICAM-1 values (102.2±35.3U/ml) at the time of diagnosis were significantly increased compared with those in the regressive disease group (disappeared or regressed within 2 years) (46.4±12.6U/ml). However, there was no significant difference in SACE activity of the regressive and progressive disease groups. Fifteen patients with a high value of circulating sICAM-1 (> 75U/ml, mean of controls+2s.d.) all had progressive disease, while only 15 of 44 patients with a high value of SACE had progressive disease. Circulating sICAM-1 will be a useful blood marker to predict outcome and to monitor disease activity in sarcoidosis.     

Circulating adhesion molecules in sarcoidosis.

Sarcoidosis is a disease of unknown etiology characterized by non-caseating granulomata together with a number of systemic abnormalities. We have recently shown these include increased expression of the integrins CD11/CD18 on peripheral blood leucocytes. Here we have measured serum levels of the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), E-selectin and vascular cell adhesion molecule-1 (VCAM-1) in 23 patients and 14 normal controls using antigen capture sandwich ELISAs. Median circulating E-selectin levels in the patients were nearly three times those of the controls (P < 0.0001, Mann-Whitney U-test), whilst ICAM-1 but not VCAM-1 levels were only slightly elevated. These results show that endothelial cell activation and shedding of E-selectin into the circulation are additional features of the pathology of sarcoidosis.     

Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression and function on cultured human glomerular epithelial cells.

Glomerular epithelial cells are involved in extracapillary inflammation (crescents) but the mechanisms of this extracapillary accumulation of macrophages, epithelial cells and occasional lymphocytes are unknown. Human glomerular parietal epithelial cells express ICAM-1 and VCAM-1 on immunohistological stains of renal biopsies. We studied the expression of these cell adhesion molecules on cultured human glomerular epithelial cells (HGEC), their regulation by pro-inflammatory cytokines, and their role in mediating the adhesion of concanavalin A (Con A)-activated peripheral blood mononuclear cells. Human glomerular epithelial cells in culture constitutively express ICAM-1 and VCAM-1. The expression of ICAM-1 was not significantly altered by tumour necrosis factor-alpha (TNF-alpha) (P = 0.32), IL-1 beta (P = 0.24), interferon-gamma (IFN-gamma) (P = 0.66) or IL-4 (P = 0.85). VCAM-1 expression was increased by all four cytokines, but only significantly so by IL-4 (P = 0.0001). Con A-stimulated, monocyte-depleted peripheral blood lymphocytes bound to human glomerular epithelial cells, median 28.9% (range 14.5-37.9%). This adherence was significantly inhibited by anti-ICAM-1 (P = 0.03) and anti-LFA-1 (P = 0.02), but not by anti-VCAM-1 (P = 0.13) or by antibody to von Willebrand factor (P = NS). The interaction between ICAM-1 on HGEC and LFA-1 on mononuclear cells may be important in the pathogenesis of extracapillary inflammation in glomerulonephritis.     

Soluble endothelium-associated adhesion molecules in patients with Graves' disease.

The targeting and recruitment of inflammatory cells to vascular endothelium in Graves' disease (GD) is mediated by intercellular adhesion molecule-1 (ICAM-1), endothelial leucocyte adhesion molecule-1 (ELAM-1), and vascular cell adhesion molecule-1 (VCAM-1). We have studied serum levels of soluble ICAM-1 (sICAM-1), soluble ELAM-1 (sELAM-1), and soluble VCAM-1 (sVCAM-1) in patients with GD (n = 21) and in patients with iodine-deficient goitre (IDG) (n = 23). The serum levels of sICAM-1 were markedly elevated in patients with GD before treatment with thiamazole (median 560 ng/ml versus 185 ng/ml in patients with IDG). In addition, elevated serum concentrations of sELAM-1 (median 85 ng/ml versus 33 ng/ml, respectively) and sVCAM-1 (median 42 ng/ml versus 15 ng/ml, respectively) were observed in patients with GD (P < 0.01 for all). The serum levels of sELAM-1 and sVCAM-1 dropped significantly after initiation of therapy and were within the normal range after 4, and 8 weeks of therapy, respectively. Serum levels of sICAM-1 were elevated even after 8 weeks of therapy. Serum levels of sVACM-1 and sICAM-1 correlated with the serum concentrations of anti-thyroid-stimulating hormone (TSH)-receptor antibodies (TSHR-R) (n = 21; r = 0.929 and r = 0.810, respectively) and anti-thyroid peroxidase antibodies (TPO-Ab) (n = 21; r = 0.673 and r = 0.750, respectively). However, no correlation between sELAM-1 and TPO-Ab, TSHR-R, and anti-thyroglobulin antibodies (Tg-Ab), respectively, could be found. In addition to thyroid hormones and autoantibodies, serum concentrations of sELAM-1 and sVCAM-1, but not sICAM-1, could be useful as clinical markers for disease activity.     

氯沙坦对实验兔颈动脉粥样硬化和血清ICAM-1、VCAM-1的影响

目的:观察氯沙坦对动脉粥样硬化程度和黏附分子的影响.方法:将24只雌雄各半新西兰白兔随机均分为对照组、高脂组、治疗组.对照组喂普通饲料,高脂组喂以高脂饲料,治疗组为高脂饲料加用氯沙坦25mg/(kg·d).分别于实验开始前、开始后第4、8、12周清晨空腹取各组实验动物耳中央静脉血0.5ml,分别测定并比较各组空腹状态下...     

螺内酯对DM2大鼠肾脏保护及ICAM-1表达的影响

目的:观察螺内酯对2型糖尿病(DM2)大鼠血、尿细胞间黏附分子-1(intercellular adhesion molecule-1,ICAM-1)的表达及肾脏组织结构和功能的影响.方法:将30只健康SD雄性大鼠随机分为正常对照组(NC组)n=10,DM2模型组(DM组)n=10,DM2模型+螺内酯治疗组(SPI组)...     

黏附分子与冠状动脉病变程度的相关性分析

探讨黏附分子与冠状动脉病变程度的关系。分析 88例冠状动脉造影患者临床资料 ,并经ELISA法检测患者循环血中可溶性细胞间黏附分子 1(sICAM 1)、可溶性血管细胞黏附分子 1(sVCAM 1)、P选择素 (P selectin)水平。结果sICAM 1、sVCAM 1和P selectin在冠心病患者循环血中明显增高 ,与病变严重程度有一定关系 ;P selectin在急性冠状动脉综合征患者中 [( 3 8 76± 6 74) μg L) ]明显增高 ,与对照组 [( 19 5 4± 1 72 ) μg L]间有非常显著性差异(P <0 0 1) ;sICAM 1与低密度脂蛋白呈正相关 (r=0 2 71,P <0 0 5 ) ;sVCAM 1与年龄和胆固醇呈正相关 (r =0 2 84,P <0 0 5 ;r=0 3 69,P <0 0 1)。提示循环血中黏附分子水平可反映出动脉粥样硬化病变的炎症反应状态。可作为估计冠状动脉粥样硬化病变严重程度的指标之一     

兔高脂血症与血管内皮功能的关系

目的 观察一氧化氮(NO)和细胞间黏附分子-1(ICAM-1)在高脂血症及动脉粥样硬化(AS)动物模型中的表达,探讨高脂血症及AS与血管内皮功能和ICAM-1的关系.方法 采用高脂饮食饲养家兔建立高脂血症和AS动物模型,正常饮食组为对照组;两组动物于0、8和16周分别取静脉血,检测血清中胆固醇(TC)、低密度脂蛋白(LDL)、NO和ICAM-1水平,并观察TC和LDL与NO和ICAM-1的相关性;16周后处死动物,免疫组化法和RT-PCR检测ICAM-1在主动脉粥样硬化斑块中的表达.结果 饲养8周时,高脂饮食组血清TC和LDL明显增加(P＜0.01),NO和ICAM-1无明显变化;饲养16周时,NO水平明显下降(P＜0.01),ICAM-1水平明显增高(P＜0.01).TC和LDL与NO呈负相关,与ICAM-1呈正相关.结论 高脂血症及AS造成血管内皮功能失调,导致NO和ICAM-1的异常表达;NO和ICAM-1参与了AS的形成.     

Intercellular adhesion molecule-1 expression by macrophages in human gastrointestinal carcinoma: Possible roles as host immune/inflammatory reaction

Tumor-associated macrophages (TAM) are one of the factors which modulate the carcinoma progression. The present study described immunohistochemical expression of intercellular adhesion molecule-1 (ICAM-1) in stromal cells in human gastrointestinal carcinoma identifying the cell types by immunoelectron microscopy. In colon and gastric carcinomas, ICAM-1-positive cells were mostly stromal cells, and major cell types were identified as macrophages and fibroblasts by immunoelectron microscopy. Macrophages were characterized by their ovoid shape, cytoplasmic projections, abundant vacuoles, phagocytosis, and paucity of rough endoplasmic reticulum. Fibroblasts contained stacks of rough endoplasmic reticulum. Macrophages were major cells among ICAM-1-positive cells along the invasive margin, while fibroblasts were predominant in the stroma within carcinoma in colon and intestinal-type gastric carcinomas. Lymphocytes positive for lymphocyte function associated antigen (LFA-1), a counter-receptor of ICAM-1, were densely distributed along the invasive margin, and sparsely in the stroma within carcinoma. In diffuse-type gastric carcinoma, most macrophages were dendriticshaped and negative for ICAM-1. Our study suggests that the invasive margin is an area similar to active inflammation, where the antigen presenting cells (macrophages) and lymphocytes may interact via the ICAM-1/LFA-1 adhesion.