ACS患者体内同型半胱氨酸与黏附分子CD11b/CD18的相关性

目的:探讨急性冠脉综合征患者体内血浆同型半胱氨酸（HCY）与全血白细胞黏附分子CD11b/CD18水平的变化及其相关性。方法:对急性冠脉综合征（ACS）患者53例与健康人35例采用酶联免疫法测定血浆HCY水平,通过流式细胞仪采用直接免疫荧光法测定白细胞黏附分子CD11b/CD18的表达。结果:ACS组血浆HCY水平显著高于对照组,分别为29.1±13.5和12.7±6.9μmol/L（P<0.01）,ACS组白细胞表面CD11b/CD18表达水平显著高于对照组,分别为6.0±2.3比4.3±1.6 MFI（P<0.05）,27.7±7.7比19.6±4.9 MFI（P<0.05）。HCY水平与CD11b、CD18的表达显著相关。结论:同型半胱氨酸作为炎症介质可能通过调节白细胞黏附分子CD11b/CD18的表达,在ACS发生和发展中起重要作用。     

急性冠状动脉综合征病人同型半胱氨酸和黏附分子的改变

目的探讨急性冠状动脉综合征(acute coronary syndrome,ACS)病人体内血浆同型半胱氨酸(homocysteine,Hcy)、分化群(cluster of differentiation antigen,CD)11b/CD18、C反应蛋白(C-reactive protein,CRP)和白细胞计数的改变。方法选择ACS75例、稳定型心绞痛(stabe angina pectoris,SAP)35例,健康人35名为对照组,用酶联免疫法测定血浆Hcy,采用直接免疫荧光法用流式细胞仪测定CD11b与CD18表达,比较CRP、白细胞计数、血糖、血脂和血压改变。结果①ACS组和SAP组的血糖、总胆固醇、低密度脂蛋白-胆固醇均高于对照组,而高密度脂蛋白胆固醇则低于对照组;而在ACS组和SAP组差异无统计学意义;ACS组收缩压和舒张压均高于对照组;②ACS组血浆Hcy(19±11)#mol/L、CD11b和CD18表达分别为(6.0±2.3)MC(平均荧光强度单位)和(27.7±4.3)MC,白细胞计数为(9.4±2.4)×109/L均高于SAP组(P<0.05)。CRP为3.75(0.5～7)mg/L,与SAP组比较,差异无统计学意义;SAP与对照组比较,仅Hcy轻度升高和CRP升高,余差异无统计学意义。结论ACS和SAP有血脂、血糖、血压改变,同时Hcy、白细胞计数及CD、CRP升高,表明炎性因素可能参与冠心病的发生。     

冠心病患者白细胞膜黏附分子CD11b/CD18表达的研究

目的探讨冠心病患者中性粒细胞和单核细胞膜黏附分子CD11b/CD1s的表达.方法对60例冠心病患者(冠心病组)采用流式细胞仪直接免疫荧光法与20例正常者(正常组)比较检测中性粒细胞和单核细胞膜黏附分子CD11b/CD18的表达.结果冠心病组中性粒细胞和单核细胞膜黏附分子CD11b/CD18表达较正常组均增加,有显著性差异(P＜0.05),环磷酸腺苷葡胺对不稳定性心绞痛患者干预后,其表达显著增高,有极显著性差异(P＜0.01).结论冠心病患者中性粒细胞和单核细胞膜黏附分子CD1tb/CD18表达明显增加,其增加程度与心肌缺血的类型有关.     

急性冠脉综合征患者血清E-选择素和白细胞CD11b/CD18表达的研究

目的观察血清E-选择素水平、中性粒细胞及单核细胞CD11b/CD18表达在急性冠脉综合征(ACS)患者中的变化,探讨其与斑块稳定性的关系.方法 30例ACS患者(ACS组)、24例稳定型心绞痛患者(SA组),30例冠状动脉造影阴性者作为对照组.酶联免疫吸附法检测E-选择素,流式细胞仪检测CD11b/CD18的表达.结果血清E-选择素水平、中性粒细胞和单核细胞膜CD11b/CD18的表达ACS组显著高于SA组(P<0.01)和对照组(P<0.01).结论 ACS患者血清E-选择素水平、中性粒细胞和单核细胞膜CD11b/CD18的表达增加与斑块不稳定性有关.     

冠心病患者PTCA手术前、后CD11b/CD18的表达及临床意义

探讨不同类型 CHD患者白细胞粘附分子的变化和 PTCA对白细胞粘附分子表达的影响。选择行冠状动脉造影 （CA）和 PTCA术的患者 2 7例 ,将其分为 SAP组、UAP组及正常对照组。分别检测 CA或 PTCA术前、术后 6h,2 4h,48h的白细胞计数及 CD11b/ CD18在单核细胞和中性粒细胞 （PMN）膜上的表达。结果 :1CHD患者血液中单核细胞、PMN的 CD11b/ CD18表达较健康对照组均显著增加 （P<0 .0 1） ,其中 U AP组最为明显。 2 PTCA术后白细胞计数和单核细胞 CD11b/ CD18表达与术前无明显差异 ,而 PMN膜 CD11b/ CD18表达在 6 h开始升高 （P<0 .0 1） ,48h升高尤为显著。而 CA术前后各项检测指标均无差异。结论 :CHD患者 PMN、单核细胞膜上 CD11b/CD18的表达明显增加 ,粘附性增强 ,其增加程度与心肌缺血状态有关 ;PTCA术后 PMN膜 CD11/ CD18表达的上调 ,可能是冠脉再狭窄的原因之一。     

生血宁片对肿瘤坏死因子α诱导的白细胞活化的影响及相关机制

目的探讨生血宁片对肿瘤坏死因子α(TNF-α)诱导的白细胞活化的影响和相关机制。方法采集志愿者血液后提取并培养外周血中性白细胞,分为空白对照组,TNF-α组,1μmol/L生血宁片组、10μmol/L生血宁片组、100μmol/L生血宁片组。分别用细胞黏附实验和Transwell小室法观察生血宁片对20 ng/ml TNF-α诱导的中性白细胞黏附和跨膜迁移能力的影响;流式细胞术检测中性白细胞表面黏附分子(CD11b、CD18)的表达情况。结果 TNF-α组明显提升中性白细胞活性,黏附能力明显强于空白对照组(P<0.01);10、100μmol/L生血宁片组的中性白细胞黏附能力均明显低于TNF-α组(P<0.05)。TNF-α组中性白细胞跨膜迁移力明显强于空白对照组(P<0.01);10、100μmol/L生血宁片组的中性白细胞游出数均明显低于TNF-α组(P<0.05)。TNF-α组CD11b和CD18的表达量均明显高于空白对照组(P<0.01);生血宁片对CD11b和CD18的表达量抑制作用呈剂量依赖性,10、100μmol/L生血宁片组的CD11b和CD18的表达量均明显低于TNF-α组(P<0.05)。结论生血宁片可通过抑制白细胞表面黏附分子CD11b、CD18的表达来抑制TNF-α诱导的白细胞活化。     

冠心病心绞痛患者血浆IL-8水平和中性粒细胞CD11 b/CD18 表达与冠状动脉狭窄程度及病变稳定性的相关性

目的 :探讨冠心病心绞痛患者血浆白细胞介素 8(IL 8)水平和中性粒细胞CD11b/CD18表达与冠状动脉狭窄程度和病变稳定性的关系。方法 :选择 6 8例不稳定型心绞痛患者 (UA组 )和 5 2例稳定型劳累性心绞痛患者 (SA组 ) ,用夹心ELISA法测定IL 8水平 ;用流式细胞仪检测其CD11b/CD18受体表达。同期测定 2 0例正常人以作对照。依据冠状动脉造影结果 ,按直径法和ABC分型综合评定心绞痛患者冠状动脉病变程度。结果 :UA组患者血浆IL 8为 (10 0 .11± 31.89)ng/L ,显著高于SA组患者〔(5 9.0 8± 19.2 9)ng/L ,P <0 .0 1〕和正常对照组〔(47.6± 2 0 .8)ng/L ,P <0 .0 1)〕 ;CD11b/CD18表达UA组患者 (433± 6 1)也显著高于SA组患者 (2 4 0± 5 3,P <0 .0 1)和对照组 (2 2 5± 37,P <0 .0 1)。UA组患者血浆IL 8和CD11b/CD18表达在A型、B型及C型病变组依次增加 ,并与冠状动脉狭窄直径呈正相关 (r =0 .6 72 3,P <0 .0 0 1和r =0 .5 5 94 ,P <0 .0 0 1)。SA组上述参数与正常对照组比较以及在A、B、C 3种病变组之间比较均无统计学差异。结论 :心绞痛患者血浆IL 8和CD11b/CD18表达增加与冠状动脉狭窄程度和病变稳定性有关。     

槲皮素对急性心肌梗死大鼠模型白细胞黏附分子表达的影响

目的研究槲皮素对急性心肌梗死(AMI)大鼠白细胞黏附分子CD11b/CD18表达的影响。方法采用大鼠急性心肌梗死模型,用流式细胞仪测定白细胞表面黏附分子CD11b的表达。同时测定肌酸激酶(CK)、乳酸脱氢酶(LDH)、丙二醛(MDA)和超氧化物歧化酶(SOD)。结果大鼠急性心肌梗死后白细胞表面黏附分子CD11b平均荧光强度增高,血液中CK、LDH、MDA升高,SOD降低(P<005),槲皮素05、10mg/kg使CD11b平均荧光强度降低,降低CK、LDH、MDA,提高SOD含量(P<001)。结论槲皮素通过抑制细胞间黏附分子表达对AMI后的心肌损伤具有保护作用。     

冠心病患者中性粒细胞和单核细胞CD11b/CD18表达的研究

目的 :探讨不同类型冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达的变化。方法 :选择经冠状动脉造影确诊的 49例心绞痛患者 ,30例急性心肌梗死患者和 2 0例正常人 ,用流式细胞仪直接免疫荧光法检测中性粒细胞和单核细胞膜 CD11b/CD18表达。结果 :冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达较正常对照组均显著增加 （P<0 .0 1） ;不稳定性心绞痛和急性心肌梗死患者中性粒细胞和单核细胞膜 CD11b/CD18表达显著高于稳定性心绞痛患者 （P<0 .0 1）。与正常对照组比较 ,心绞痛患者组中性粒细胞和单核细胞计数无变化 （P>0 .0 5 ） ,而急性心肌梗死组明显增加 （P<0 .0 1）。急性心肌梗死患者中性粒细胞和单核细胞膜 CD11b/CD18表达与梗死范围无关。结论 :冠心病患者中性粒细胞和单核细胞膜 CD11b/CD18表达明显增加 ,其增加程度与心肌缺血的类型有关。     

急性动脉血栓患者中性粒细胞黏附分子表达的变化及意义

目的探讨急性动脉血栓形成患者中性粒细胞(PMN)表面黏附分子CD62L和CD11b/CD18的表达及其意义。方法选择急性心、脑动脉血栓患者各20例,健康志愿者30例作为对照组。运用流式细胞仪检测外周血中PMN表面黏附分子CD62L和CD11b/CD18表达。结果相对于正常组黏,动脉血栓组黏附分子CD62L平均抗体阳性表达率显著降低(P<0.001);CD11b/CD18平均阳性表达率显著升高(P<0.001)。动脉血栓组内部CD62L、CD11b/CD18相关分析,二者呈明显负相关(r=-0.259,P<0.001)。结论在动脉血栓的急性期,以细胞黏附为表现的PMN活化加快了血栓的进程,可能是血栓形成的重要发病原因之一。     

Reduced CD43 expression on the neutrophils of MDS patients correlates with an activated phenotype of these cells

CD43 (also known as leukosialin and sialophorin) is a surface sialoglycoprotein expressed at high levels on most leukocytes implicated in adhesion, antiadhesion, and activation/proliferation mechanisms. We studied the expression of this molecule on the leukocytes of patients with myelodysplastic syndromes (MDSs) in an effort to detect acquired deficiencies of this molecule. We used immunofluorescence flow cytometry in analyzing whole blood and isolated neutrophils from 49 MDS patients, 33 men and 16 women aged 33 to 85 years (median, 75 years), and 18 healthy individuals aged 35 to 80 years (median, 72 years). According to French-American-British classification criteria, 13 patients had refractory anemia, 18 had refractory anemia with ringed sideroblasts, 9 had refractory anemia with excess of blasts, 4 had refractory anemia with excess of blasts in transformation to acute leukemia, and 5 had chronic myelomonocytic leukemia. We found decreased expression of CD43 on the neutrophils of these patients, and we correlated this finding with the activation status of these cells as it is defined by their phenotypes. We studied the expression of CD11b, CD18, CD35, CD67, CD69, CD44, and CD53 molecules known to be changed in the activated form of neutrophils. CD43 expression correlated positively with CD53 and CD44 expression and negatively with CD11b, CD18, CD35, CD67, and CD69 expression. Additionally, increased levels of soluble vascular cell adhesion molecules were detected in these patients, suggesting endothelial cell activation. In conclusion, we believe that the decreased expression of CD43 on the neutrophils of MDS patients is associated with activation of these cells and is probably due to cleavage of the molecule from the cell surface and that the same mechanism is possibly responsible for the parallel down-regulation of CD44 and CD53.     

肿瘤坏死因子、白细胞介素8、可溶性细胞间粘附分子1和CD11b/CD18在良恶性胸腔积液的价值

目的 研究结核性及恶性胸腔积液患者及血清中肿瘤坏死因子（TNF）、白细胞介素－8（IL－8）、胸液中可溶性细胞间粘附分子1（sICAM-1）及外周血多形核白细胞（PMN）上粘附分子CD11d/CD18在参与胸膜病变的病理生理过程中的作用和在鉴别诊断上的价值。方法 采用放射免疫分析法（RIA法）、双抗体夹心ELISA法及流式细胞仪技术,检测31结核性、31例恶性胸腔积液患者胸液和（或）血清中TNF、IL－8、sICAM－1和CD11d/CD18表达水平,并与31例健康献血者对照。结果 结核性和恶性胸腔积液患者血清中TNF、IL－8含量以及PMN上CD11d/CD18表达显著高于正常对照组（P＜0．01）, 结核性胸液中TNF与IL－8水平和血PMN上CD11d/CD18表达明显高于恶性胸液患者（P＜0．01）,结核性胸粹中sICAM－1水平明显低于恶性胸液（P＜0．01）。胸腔积液中TNF与IL－8、sICAM－1水平呈显著正相关（r＝0．74和r＝0．79,P＜0．01）,血清TNF与PMN上CD11d/CD18的表达呈显著正相关（r＝0．61,P＜0．01）,胸腔积液中sICAM－1水平与血PMN上CD11d/CD18的表达呈显著负相关（经作曲线拟合,Y=1442．31－36．85X∧2＋0．25X∧2,R∧2＝0．59,F＝19．83,P＜0．01）。结论 细胞因子TNF、IL－8和粘附子sICAM－1、CD11b/CD18相互联系,在结核和肿瘤性胸膜病变的免疫 理生理过程中起着重要作用。它们在结核性和肿瘤性胸腔积液患者的表达水平不同,可作为临床上鉴别诊断的参考指标。     

Decrease in adhesion molecules on polymorphonuclear leukocytes of patients with fibromyalgia

Fibromyalgia (FM) is a chronic widespread pain condition in highly stressed humans. Because stress is known to modulate adhesion molecule expression, we determined L-selectin (CD62L) and β₂-integrin (CD11b/CD18) expression on the surface of polymorphonuclear leukocytes in 22 patients with FM. As compared to age and sex-matched healthy controls, FM patients showed a significantly decreased expression of CD62L (p < 0.01) and CD11b/CD18 (p < 0.05) on polymorphonuclear leukocytes. These changes might lower the rate of polymorphonuclear leukocyte migration to sites of inflammation and thereby compromise defense against infections and pain control.     

Monoclonal antibodies to leukocyte integrins CD11a/CD18 and CD11b/CD18 or intercellular adhesion molecule-1 inhibit chemoattractant-stimulated neutrophil transendothelial migration in vitro.

Intercellular adhesion molecule-1 (ICAM-1) is present on the endothelium and binds to one or more members of the CD11/CD18 family of leukocyte surface integrins. To assess the role of these molecules in mediating chemotaxis of neutrophils across the endothelium, an in vitro model consisting of monolayers of human umbilical vein endothelial cells (HUVEC) grown on amniotic connective tissue was used. Neutrophils placed on the apical sides of these cultures migrated across the endothelium in response to chemoattractants added basally. Monoclonal antibodies (MoAbs) to CD11a, CD11b, and CD18 on the neutrophils inhibited this migration by 52% +/- 11%, 29% +/- 19%, and 90% +/- 7%, respectively. An MoAb to ICAM-1 inhibited transendothelial chemotaxis of the leukocytes by 55% +/- 16%. Inhibition was mediated by binding of the MoAb to ICAM-1 on the HUVEC, rather than by any direct effect of the antibody on the neutrophils. When used in combination, MoAbs to CD11a and to CD11b inhibited migration in a nearly additive fashion. A similar additive effect was observed when MoAbs to CD11b and to ICAM-1 were used together. In contrast, MoAbs to CD11a and to ICAM-1 produced no more inhibition when used in combination than when added singly. These results show that ICAM-1, CD11a/CD18, and CD11b/CD18 all participate in controlling migration of neutrophils across endothelial monolayers in response to chemotactic agents.     

Active MAC-1 (CD11b/CD18) on DCs inhibits full T-cell activation

The beta2 integrins are important for transendothelial migration of leukocytes as well as for T-cell activation during antigen presentation. Despite abundant expression of beta2 integrins on antigen-presenting cells (APCs), their functional relevance for antigen presentation is completely unclear. We show here that dendritic cells (DCs) from CD18-deficient mice, which lack all functional beta2 integrins, have no defect in antigen presentation. Moreover, DCs from normal mice express inactive beta2 integrins that do not become activated on contact with T cells, at least in vitro. Pharmacologic activation of beta2 integrins on DCs results in a significant reduction of their T cell-activating capacity. This effect is mediated by Mac-1 (CD11b/CD18) on DCs because it could be reversed via blocking antibodies against CD18 and CD11b. Furthermore, the antigen-presenting capacity of macrophages, which express constitutively active beta2 integrins, is significantly enhanced on Mac-1 blockade. We therefore conclude that active CD11b/CD18 (Mac-1) on APCs directly inhibits T-cell activation.     

冠心病血瘀证病人血白细胞CD11b/CD18表达的研究

目的 :探讨不同类型冠心病病人中性粒细胞和单核细胞CD11b/CD18表达的变化规律及其与冠心病中医证型之间的关系。方法 :采用流式细胞仪检测不同类型和不同中医证型冠心病中性粒细胞和单核细胞CD11b/CD18表达。结果 :UAP和AMI组中性粒细胞和单核细胞显著高于SAP组 (P <0 .0 0 1)。SAP、UAP、AMI组之间中性粒细胞和单核细胞CD11b、CD18表达随着病情严重程度增加而明显增加(P <0 .0 0 1)。AMI组中性粒细胞和单核细胞CD11b、CD18的表达 ,血瘀证组明显高于非血瘀证组 (P <0 .0 0 1)。结论 :冠心病病人中性粒细胞和单核细胞CD11b/CD18表达明显上调 ,其增加程度与心肌缺血的类型及冠心病中医血瘀证有关。     

Persistence of high CD40 and CD40L expression after restorative proctocolectomy for ulcerative colitis

AIM:To focus on the role of CD40 and CD40L in their pathogenesis. METHODS:We analyzed by immunohistochemistry the CD40 and CD40L expression in the pouch mucosa of 28 patients who had undergone RPC for UC, in the terminal ileum of 6 patients with UC and 11 healthy subjects. We also examined by flow cytometry the expression of CD40 by B lymphocytes and monocytes in the peripheral blood of 20 pouch patients, 15 UC patients and 11 healthy controls. RESULTS:Ileal pouch mucosa leukocytes presented a significantly higher expression of CD40 and CD40L as compared to controls. This alteration correlated with pouchitis, but was also present in the healthy pouch and in the terminal ileum of UC patients. CD40 expression of peripheral B lymphocytes was significantly higher in patients with UC and pouch, respect to controls. Increased CD40 levels in blood B cells of pouch patients correlated with the presence of spondyloarthropathy, but not with pouchitis, or inflammatory indices. CONCLUSION:High CD40 expression in the ileal pouch mucosa could be implied in the pathogenesis of pouchitis following proctocolectomy for UC, whereas its increased levels on peripheral blood B lymphocytes are associated with the presence of extraintestinal manifestations.     

Overexpression of complement receptors and related antigens on the surface of bone marrow mast cells in patients with systemic mastocytosis

Depending on their stage of maturation and other factors, mast cell (MC) subsets differ from each other in terms of the expression of complement-associated antigens. This study analysed the expression of various complement-related cell surface antigens (CD11b/CR3, CD11c/CR4, CD35/CR1, CD55/DAF, CD59/MIRL, CD88/C5aR) on bone marrow mast cells (BMMC) in patients suffering from systemic mastocytosis (SM), other haematological diseases and non-haematological disorders (control groups). Expression of complement-associated cell surface antigens was analysed by flow cytometry. There were clear immunophenotypic differences between BMMC obtained from patients with SM and those from the control subjects: the percentage of patients expressing surface CD11c, CD35 and CD88 was significantly higher in patients with SM (76%, 100%, 54%) than in the control subjects (58%, 11%, 18%) (P < 0.05). In addition, the levels of CD11c, CD35 and CD88 expressed per MC (sites per cell) were significantly higher (P < 0.05) in SM than in the control group. Expression of the complement regulatory molecules CD55 and CD59 was detected in BMMC in all patients analysed. However, the levels of CD59 per BMMC were higher in patients with SM as compared with the control subjects, which could help to explain the formation of BMMC aggregates in the former group of individuals. Together, our results showed that BMMC in systemic mastocytosis overexpressed the cell surface membrane receptors involved in binding of complement components and complement-mediated cell activation. Whether this pathological expression of complement receptors is of pathophysiological significance remains to be determined.