白细胞与内皮细胞的粘附

白细胞与内皮细胞相互作用由粘附分子介导.整合素、免疫球蛋白及选择素家族的粘附分子在这两种细胞的粘附中起关键作用.粘附的起始阶段由选择素介导,随后由CD11/CD18复合物与ICAM-1形成更为紧密的结合.多种细胞因子及炎症反应可诱导粘附.抗粘附分子单抗、药物等可抑制粘附.     

血管壁剪切应力系统及用于内皮细胞与白细胞粘附的研究

本文建立了对血管壁上的内皮细胞施加剪切应力的系统。通过对系统中的血管内流场分析表明,该系统中的血管段的中间部分作为研究剪切应力对内皮细胞作用,以及研究内皮细胞与其它细胞粘附力的场所是比较理想的。采用该系统对在体内皮细胞研究发现：当对内皮细胞施加２８ｄｙｎ／ｃｍ２的剪切应力时,内皮细胞并未出现暴发性释放前列环素的现象,前列环素释放水平略有升高（０．４１±０．０５ｎｇ／ｃｍ２ｍｉｎ）以后呈线性下降并稳定在一定水平上（０．１７±０．０４ｎｇ／ｃｍ２ｍｉｎ）。在２８ｄｙｎ／ｃｍ２剪切应力下,受机械损伤的内皮细胞和动脉粥样硬化的内皮细胞仍能与较多白细胞粘附,而在正常内皮细胞和去掉内皮细胞的动脉壁几乎无白细胞粘附,说明在内皮细胞受损或动脉粥样硬化时,内皮细胞与白细胞的粘附增强     

几种不同刺激对血管内白细胞粘附的影响

目的：研究几种刺激引起白细胞与内皮细胞粘附的变化。方法：本实验采用脉冲电刺激、缺血再灌、内毒素和白介素-8等物理或药物的作用,观察大鼠肠系膜细静脉内白细胞粘附及白细胞和血管内皮粘附之间的差别。结果：缺血再灌、内毒素、内毒素、脉冲电刺激和白介纱-8（IL-8）作用后肠系膜细静脉白细胞粘附数量比正常组明显增多,IL-8用药后30min细静脉内白细胞粘附数量最多、缺血再灌、内毒素、脉冲电刺激后白细胞粘附数量大致相同。结论：缺血再灌、内毒素、脉冲电刺激能诱导白细胞的粘附作用。造成内皮损伤,IL-8诱导白细胞的粘附作用最强。     

内毒素血症大鼠肠道内毒素移位的研究

肠源性内毒素血症是多器官功能衰竭的重要发病因素之一,但肠源性内毒素血症的发病机理迄今尚未阐明,本工作在离体动物,离体大鼠回肠血管灌流标本和分离的小肠粘膜刷状缘微囊制备上,观察到循环血中内毒素正反馈地促进肠道内毒素移位,多种调节肽参与内毒素移位的调控,内皮素促进而心钠素抑制其移位过程,肠道内毒素的移位主要不是通过跨细胞途径,本工作还发现牛磺酸具有抑制肠道素移位,改善内毒素血症动物预后的作用,提示牛磺     

大鼠肝癌诱发过程中血浆对红细胞与血管内皮细胞粘附的影响

在大鼠肝癌诱发过程中,为了分析自体血浆对红细胞与内皮细胞粘附的影响,采用红细胞计数及透光度的改变来检测不同时相粘数的变化。结果显示自体血浆能明业增强红细胞与内皮细胞的粘附作用。     

缺氧复合失血性休克动物血浆对血管内皮细胞与白细胞粘…

本实验观察缺氧（模拟海拔４ ０００ｍ高原２４ｈ）复合失血性休克２４ｈ山羊血浆（ＳＰ）对培养的肺动脉内皮细胞（ＰＡＥＣ）与多形核白细胞（ＰＭＮ）粘附的影响,并对其机制进行了探讨。结果表明,ＰＡＥＣ在含２５％浓度ＳＰ的培养液中孵育１０ｍｉｎ－１２ｈ后,与ＰＭＮ粘附率明显增加（２７．４％－４６％,与对照组５％相比Ｐ〈０．０１）;温育１２ｈ末ＰＡＣＥ与ＰＭＮ的粘附力也比孵育３ｈ者明显增加（Ｐ〈０．０１）;     

体外流动剪切力作用下的白细胞-内皮细胞动态粘附

建立一个用于体外研究特定流动剪切力作用下白细胞和内皮细胞动态相互作用的方法。利用建立的平板流动小室系统可在体外产生特定的流动剪切力。将培养的人脐静脉内皮细胞装入平板流动小室后 ,以 0 .71dynes/cm2 的流动剪切力把含有吖啶橙染色的白细胞的灌流液导入流动小室 ,由此产生了白细胞和内皮细胞的动态粘附过程。整个粘附过程通过OlympusIX70倒置荧光显微系统观察 ,同时通过CCD摄象头录像。然后用图象采集卡将录像采集为数字图象并保存。利用针对实验设计的图象处理和分析方法 ,对采集的数字图象进行处理和测量 ,可以得到粘附白细胞的个数和滚动白细胞的速度。通过研究内毒素脂多糖 (LPS)对内皮细胞粘附功能的促进及地塞米松 (DXM )对该刺激的抑制作用来验证。对于用内毒素脂多糖 (LPS)处理的内皮细胞 ,固定粘附和慢速滚动的白细胞的个数比对照组分别显著增加了 2 3.7倍和 4 .1倍 ,同时白细胞在粘附作用过程中慢速滚动和快速滚动的速度比对照组明显降低了 2 5 .6 %和 2 6 .1%。而对于脂多糖和地塞米松 (DXM)处理过的内皮细胞 ,上述内毒素引起的影响被显著抑制了。该方法可以用于研究不同的化学和物理刺激对内皮细胞功能的影响机制 ,及用来评价各类抑制内皮细胞粘附功能的药物。     

突然扩张流槽中血管内皮细胞表面粘附蛋白表达的研究

动脉粥样硬化的非随机分布与当地的血流动力环境有关,为了研究复杂的流体动力学条件对血和皮细胞生理功能的影响,构建了平行板式平直流槽和突然扩张流槽,通过数值模拟分析了流型的特征,并探讨流型改变对人脐静脉血管内皮细胞表面粘附蛋白表达的影响,发现突然扩张流槽中流动的空间变化使得总体细胞表面粘附蛋白ICAM－1的表达显著高于平直流槽中的均匀定常剪切作用,表明局部流动空间变化的性质可以影响血管内皮细胞的功能。     

Inhibition of neutrophil adhesion by pectic galacturonans

The inhibition of the adhesion of neutrophils to fibronectin by the fragments of the main galacturonan chain of the following pectins was demonstrated: comaruman from the marsh cinquefoil Comarum polustre, bergenan from the Siberian tea Bergenia crassifolia), lemnan from the duckweed Lemna minor), zosteran from the eelgrass Zostera marina), and citrus pectin. The parent pectins, except for comaruman, did not affect the cell adhesion. Galacturonans prepared from the starting pectins by acidic hydrolysis were shown to reduce the neutrophil adhesion stimulated by phorbol 12-myristate 13-acetate (1.625 μM) and dithiothreitol (0.5 mM) at a concentration of 50–200 μg/ml. The presence of carbohydrate chains with molecular masses higher than 300, from 100 to 300, and from 50 to 100 kDa in the galacturonan fractions was proved by membrane ultrafiltration.     

Cytokines and Cell Adhesion Molecules in Tumor-Endothelial Cell Interaction and Metastasis

Metastasis is a multistep process in which a metastatic tumor cell detaches from the primary tumor, invades the surrounding tissues, passes through supporting structures such as interstitial stroma and extracellular matrix, and enters the lymphatic or blood circulation (Poste and Fidler, 1980). Only a few of the neoplastic cells released into the circulation, that survive hemodynamic pressure and host defense mechanisms, will form metastases. The arrest of tumor cells in the capillary bed of secondary organs through an interaction with vascular or lymphatic endothelium and subendothelial basement membrane is followed by their extravasation into the tissue parenchyma, and then micro-metastasis formation. Therefore cell-cell and cell-substrate adhesions occur at different moments in this process. With the recent identification and characterization of cell surface molecules, it has become of particular interest to clarify their role in tumor progression and metastasis (Albelda, 1993).     

VCAM-1 expression and leukocyte trafficking to the CNS occur early in infection with pathogenic isolates of SIV

Abstract: This study reports on the endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) in the central nervous system (CNS) early after experimental infection of rhesus monkeys (Macaca mulatta) with pathogenic and nonpathogenic simian immunodeficiency virus (SIV). Diffuse endothelial expression of VCAM-1 was observed in the CNS in all animals receiving pathogenic SIV These findings demonstrate the rapidity with which pathogenic SIV is able to enter the CNS and induce endothelial cell activation.     

Cytokines and Cell Adhesion Molecules in Tumor-Endothelial Cell Interaction and Metastasis

Metastasis is a multistep process in which a metastatic tumor cell detaches from the primary tumor, invades the surrounding tissues, passes through supporting structures such as interstitial stroma and extracellular matrix, and enters the lymphatic or blood circulation (Poste and Fidler, 1980). Only a few of the neoplastic cells released into the circulation, that survive hemodynamic pressure and host defense mechanisms, will form metastases. The arrest of tumor cells in the capillary bed of secondary organs through an interaction with vascular or lymphatic endothelium and subendothelial basement membrane is followed by their extravasation into the tissue parenchyma, and then micro-metastasis formation. Therefore cell-cell and cell-substrate adhesions occur at different moments in this process. With the recent identification and characterization of cell surface molecules, it has become of particular interest to clarify their role in tumor progression and metastasis (Albelda, 1993).     

Probing intercellular interactions between vascular endothelial cadherin pairs at single-molecule resolution and in living cells

Vascular endothelial (VE) cadherin is the surface glycoprotein cadherin specific to the endothelium that mediates cell-cell adhesion and plays a major role in the remodeling, gating, and maturation of vascular vessels. To investigate the contribution of individual VE-cadherins to endothelial cell-cell interactions and investigate whether different classical cadherins display different kinetics and micromechanical properties, we characterize the binding properties of VE-cadherin/VE-cadherin bonds at single-molecule resolution and in living human umbilical vein endothelial cells (HUVECs). Our single-molecule force spectroscopy measurements reveal that type II VE-cadherin molecules form bonds that are less prone to rupture and display a higher tensile strength than bonds formed by classical type I neuronal (N) cadherin and epithelial (E) cadherin. The equilibrium lifetime of the VE-cadherin/VE-cadherin bond is significantly longer than formed by N-cadherin/N-cadherin bonds and E-cadherin/E-cadherin bonds. These results indicate that VE-cadherins form bonds that have kinetics and mechanical properties that are significantly different from those formed by classical type I cadherins, properties that are particularly well adapted to the barrier and adhesive functions of VE-cadherin in endothelial cell-cell junctions.     

The role of neutrophils and inflammation in gastric mucosal injury

Gastric inflammation is a highly complex biochemical protective response to cellular/tissue injury. When this process occurs in an uncontrolled manner, the result is excessive cellular/tissue damage that results chronic inflammation and destruction of normal tissue. Current evidence suggests that Helicobacter pylori (H. pylori) infection and nonsteroidal anti-inflammatory drug (NSAID) ingestion are major causative factors in the pathogenesis of gastric mucosal injury in humans. In response to H. pylori infection or NSAID, neutrophils are recruited to the site of inflammation and generate reactive oxygen and nitrogen species and proteases. However, neutrophils are not able to kill the bacteria that live in the gastric mucus, and compounds produced by activated neutrophils themselves may be potentially harmful for normal tissue. It has been shown that leukocyte-vascular endothelial cell interaction is regulated by various cell adhesion molecules, and that this interaction is directly or indirectly modified by many factors, the origin of which is H. pylori and NSAIDs. This review describes the potential role of neutrophils and neutrophil-associated inflammation for gastric oxidative stress and injury induced by H. pylori and/or NSAID.