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.     

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.     

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     

Adhesion molecules (E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)) in sera from patients with Staphylococcus aureus bacteraemia with or without endocarditis

The aim of this prospective study was to evaluate if patients with endocarditis display a more extensive endothelial activation than those with bacteraemia but without endocarditis. Sixty-five patients with blood culture-verified Staphylococcus aureus bacteraemia were included and serum samples collected on admission were analysed by enzyme immunoassays. Elevated serum concentrations of adhesion molecules were found in most of the patients with S. aureus bacteraemia. Patients with endocarditis (n = 15) showed significantly higher serum E-selectin (median 156 ng/ml) and VCAM-1 (median 1745 ng/ml) concentrations compared with those with S. aureus bacteraemia but without endocarditis (80 ng/ml and 1172 ng/ml, respectively; P = 0.01 and P = 0.003). No significant difference was found between the groups concerning ICAM-1 (median 451 ng/ml versus 522 ng/ml). In addition, serum tumour necrosis factor-alpha (TNF-alpha) concentrations were significantly correlated (P < 0.002) to serum levels of E-selectin, ICAM-1 and VCAM-1.     

Inhibition of endothelial cell adhesion molecule expression with SJC13, an azaindolidine derivative,in vitro

Stimulation of cultured human umbilical vein endothelial cells (HUVEC) with lipopolysaccharide (LPS) induces adherences for human promyelocytic cell line HL60. Adherence of HL60 cells to HUVEC stimulated with LPS for 4h was completely inhibited by pretreatment with SJC13, an azaindolidine derivative. The mechanism whereby SJC13 inhibits the adhesiveness of HUVEC was investigated. Pretreatment of SJC13 inhibited LPS-induced expression of E-selectin and vascular cell adhesion molecule-1 (VCAM-1), but not intercellular adhesion molecule-1 (ICAM-1), in HUVEC, determined by flow cytometry and cellular enzyme-linked immunosorbent assay (cell-ELISA). The inhibitory activity was concentration dependent between 62.5 and 1,000 g/ml. SJC13 also selectively inhibited LPS-induced increases in E-selectin and VACM-1 mRNAs, indicating that the action of SJC13 is to inhibit synthesis of these molecules. These data demonstrate that SJC13 is capable of selectively inhibiting the expression of E-selectin and VCAM-1, but not ICAM-1, in endothelial cells.accepted by I. Ahnfelt-Rønne     

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.     

Effect of palmitic acid and linoleic acid on expression of ICAM-1 and VCAM-1 in human bone marrow endothelial cells (HBMECs)

Introduction

The amount and type of fatty acids (FAs) in the diet influence the risk of atherosclerosis. Palmitic acid and linoleic acid exist at high levels in Iranian edible oils. In this study, we investigated the effect of palmitic acid and linoleic acid on expression of soluble and cell-associated forms of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in human bone marrow endothelial cells (HBMECs).

Material and methods

The endothelial cells were induced with bacterial lipopolysaccharide (LPS) or tumor necrosis factor α (TNF-α), and thereafter incubated with palmitic or linoleic acid. The level of soluble and cell-associated VCAM-1 and ICAM-1 were analyzed using ELISA and western blot.

Results

Our findings indicated that palmitic acid up-regulates the expression of ICAM-1 and VCAM-1 in HBMECs when these cells are induced with TNF-α or LPS. In addition, the results suggest that linoleic acid could sustain up-regulated ICAM-1 and VCAM-1 in activated endothelial cells.

Conclusions

Chronic activation of endothelial cells in the presence of palmitic and linoleic may account for pathogenesis of cardiovascular events. These findings provide further support for the detrimental effects of these fatty acids, especially palmitic acid, in promotion and induction of cardiovascular diseases which are prevalent in the Iranian population.     

Does infection with Chlamydia pneumoniae and/or Helicobacter pylori increase the expression of endothelial cell adhesion molecules in humans?

Objective   To investigate if Chlamydia pneumoniae and/or Helicobacter pylori seropositivity is associated with elevated levels of soluble endothelial cell adhesion molecules (sCAMs) as markers of atherosclerotic activity.
Methods   Immunoglobulin A (IgA) and IgG antibodies to the two bacteria, soluble intercellular cell adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1) and E-selectin were measured in coronary heart disease (CHD) patients ( n  = 193) and age- and sex-matched controls ( n  = 193). Two different serological methods were used for the detection of Chlamydia antibodies: Labsystems microimmunofluorescence to detect species-specific C. pneumoniae antibodies and Medac's recombinant enzyme-linked immunosorbent assay to detect genus-specific lipopolysaccharide antibodies.
Results   The concentrations of sICAM-1 and E-selectin were higher in CHD patients with positive vs. negative Chlamydia lipopolysaccharide IgA ( P  = 0.044 for both). H. pylori antibodies alone did not predict raised levels of sCAMs, but in CHD patients sICAM-1 was increased with IgA seropositivity to both bacteria compared to double seronegativity ( P  = 0.034). Concentrations of sVCAM-1 were elevated in CHD patients with double IgA seropositivity compared to those with Chlamydia lipopolysaccharide IgA seropositivity alone ( P  = 0.018).
Conclusion   Our results may indicate that C. pneumoniae contributes to increased inflammation in CHD, and that this contribution is even more pronounced when present in combination with H. pylori IgA antibodies.     

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...     

人白介素- 4对牛血管内皮细胞保护作用的研究

目的:研究人白介素-4(hIL-4)对经TNF-α活化的牛主动脉内皮细胞(BAEC)的保护作用。方法:用不同浓度的hIL-4与BAEC共孵育2h后,再与4μg/L的TNF-α共孵育6h或18h。应用细胞ELISA方法,检测BAEC表面的E选择素和ICAM-1的表达;用MTT比色法测定hIL-4对BAEC活性的影响。结果:在一定浓度内用hIL-4预处理BAEC后,能明显抑制TNF-α诱导活化BAEC上的E选择素与ICAM-1的表达,并呈现一定的剂量依赖性。用MTT比色法测定BAEC活性的实验表明,各实验组BAEC的活性与对照组无明显差异性。结论:hIL-4能明显抑制TNF-α诱导活化的BAEC表达E选择素与ICAM-1;hIL-4对BAEC的正常功能具有一定的保护作用。     

MBP刺激的 PBMC培养上清对内皮细胞促进 T细胞增殖的作用

目的探讨髓磷脂碱性蛋白(MBP)刺激的PBMC培养上清作用的人脐静脉内皮细胞(HUVEC)对T细胞增殖的影响。方法用细胞免疫化学染色和FCM检测HUVEC的VCAM-1,ICAM-1和HLA-DR的表达;用MTT法测定MBP刺激的PBMC对T细胞增殖的影响。结果与对照相比较,MBP刺激的PBMC培养上清可诱导HUVEC特异表达VCAM-1和HLA-DR,上调ICAM-1的表达。经MBP作用的HUVEC可明显促进T细胞的增殖。结论MBP刺激PBMC的培养上清可引起内皮细胞结构和功能改变,促进T细胞增殖。     

Endothelium injury and inflammatory state during abdominal aortic aneurysm surgery: scrutinizing the very early and minute injurious effects using endothelial markers – a pilot study

Introduction

One of the most severe complications of repair surgery for abdominal aortic aneurysms (AAA) is acute kidney injury (AKI). Acute kidney injury is an inflammatory process whose pathogenesis involves endothelial cells (EC). The aim of this study was to assess the dynamics of endothelium injury markers measured during elective AAA surgery which might confirm the inflammatory character of AKI.

Material and methods

The study group consisted of 14 patients with AAA. We measured plasma soluble forms of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, P-selectin as well as the levels of von Willebrand factor (vWF) before, during (including intra-abdominal vein levels before and after aortic clamp removal) and within 2 days after surgery.

Results

We have found a biphasic response of ICAM-1, VCAM-1 and P-selectin with an initial fall and subsequent rise. However, only VCAM-1 changes were significant compared to its baseline value. The maximum decrease of VCAM-1 was observed in the renal vein 5 min after aortic clamp removal (335.42 ±129.63 ng/ml vs. 488.90 ±169.80 ng/ml baseline value, p < 0.05), and the highest rise 48 h after aortic clamp removal (721.46 ±333.99 vs. baseline, p < 0.05).

Conclusions

Vascular cell adhesion molecule-1 turned out to be the most sensitive indicator of EC injury and inflammatory status after AAA surgery. During AAA surgery, soluble forms of P-selectin, ICAM-1 and VCAM-1 demonstrate a biphasic response with an initial fall and subsequent rise. These soluble forms could have a modulatory effect on the development of inflammation.     

Circulating levels of vascular endothelial markers in obstructive sleep apnoea syndrome. Effects of nasal continuous positive airway pressure

Introduction

Obstructive sleep apnoea syndrome (OSAS) is an important risk factor in cardiovascular disorders. Although the exact mechanism remains to be elucidated, the endothelial dysfunction process seems to be implicated.

Material and methods

In order to test this hypothesis, blood circulating levels of endothelial markers were measured at baseline and 1 year after treatment with continuous positive airway pressure (CPAP). We studied 37 males using polysomnography: 20 subjects with OSAS and a 17-subject control group. An OSAS-validated sleep questionnaire covering the most important cardiovascular risk factors was applied to all subjects. Furthermore, patients received a complete general physical examination and biochemistry test with lipid profile. The specific markers measured were intercellular cell adhesion molecule-1 (ICAM-1), E-selectin, endothelin-1, von Willebrand factor (vWF) and plasminogen activator inhibitor-1 (PAI-1).

Results

Obstructive sleep apnoea syndrome patients presented higher circulating levels of ICAM-1, endothelin-1 and PAI-1 than the control group. On the other hand, no differences were found in E-selectin and vWF. After 1 year of CPAP treatment, there was a significant decrease in circulating levels of ICAM-1 and PAI-1. On the other hand, no differences were found in endothelin-1, E-selectin and vWF.

Conclusions

Obstructive sleep apnoea syndrome is associated with elevated levels of ICAM-1 and PAI-1 and these levels normalize after treatment with CPAP.     

维持性血液透析尿毒症患者sICAM-1和E-选择素水平的变化

目的 :测定维持性血液透析 (MHD)的尿毒症患者血浆中细胞间黏附分子 1(ICAM 1)和E 选择素的水平 ,探讨MHD患者动脉粥样硬化的病理机制。方法 :应用双抗夹心ELISA法 ,测定 10 5例MHD患者和 2 5例健康人 (对照组 )血浆中ICAM 1和E 选择素的水平 ,同时用B超测定患者颈动脉粥样硬化的情况 ,记录两组的血压并测定其血脂、血糖、血尿素和肌酐的水平。结果 :①MHD组血浆ICAM 1和E 选择素的水平均明显高于对照组 (P <0 .0 1)。MHD组中 ,有颈动脉硬化者血浆I CAM 1和E 选择素的水平明显高于无颈动脉硬化组 (分别为P <0 .0 1和P <0 .0 5)。②MHD组血浆ICAM 1与E 选择素以及与甘油三酯 (TG )均呈显著的正相关 (r值分别为0 .62及 0 .60 )。血浆ICAM 1的水平与舒张压也呈正相关(r=0 .41)。结论 :MHD患者存在明显的血管内皮功能损伤。血浆ICAM 1和E 选择素可作为MHD患者血管内皮损伤的标志物 ,其与MHD患者的动脉粥样硬化密切相关     

内毒素致新生大鼠肺组织PECAM-1表达的研究

目的探讨内毒素作用于新生大鼠后,肺组织血小板内皮细胞粘附分子-1(PECAM-1)表达的变化及可能作用.方法用脂多糖(LPS)诱发7日龄新生大鼠肺损伤以至于肺出血模型,用免疫组化和RT-PCR方法观察肺组织PECAM-1蛋白水平和mRNA水平表达的变化.结果正常新生大鼠肺组织表达较高水平的PECAM-1蛋白水平和mRNA水平,LPS作用后,肺组织PECAM-1蛋白水平和mRNA水平表达均存在逐渐下降趋势,mRNA水平的表达在给药后1h即明显下降,蛋白水平在给药后4h明显下降,至LPS作用后8h降至最低水平,24h存活大鼠PECAM-1蛋白水平和mRNA水平有所恢复,二者的变化趋势基本一致.结论正常新生大鼠肺组织表达较高水平的PECAM-1蛋白及mRNA,PECAM-1可能在新生大鼠肺出血的发病机制中有一定的作用,并且PECAM-1表达变化的调节是在转录水平.     

Oxidized forms of fibrinogen induce expression of cell adhesion molecules by cultured endothelial cells from human blood vessels

Oxidized forms of fibrinogen similarly to initial non-oxidized fibrinogen induced expression of P-selectin and ICAM-1 cell adhesion molecules in the cultured endothelial cells derived from human umbilical vein. The effect of oxidized fibrinogen on the expression of adhesion molecules was more pronounced. These data attest to more active participation of oxidized forms of fibrinogen into inflammation in the vascular wall, the first stage of atherogenesis. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 142, No. 9, pp. 277–281, September, 2006     

热射病猪血管内皮细胞损伤的病理变化及相关黏附分子表达北大核心

背景:热射病是一种死亡率极高的疾病,是由高温引起的广泛内皮细胞损伤及多脏器功能衰竭的临床综合征,常见的并发症是凝血功能异常,而血管内皮病变在重度中暑引发的凝血功能紊乱中发挥关键作用。目的:观察热射病猪血管内皮细胞损伤的病理变化特点及相关黏附分子细胞间黏附分子1的表达。方法:选取12只普通级健康雄性巴马小型猪,体质量15-20 kg,采用随机数字表法分为常温对照组及热射病组,每组6只。热射病组建立高温高湿环境下重度中暑猪模型,而常温对照组小猪置于恒温恒湿气候舱中。采集两组实验前、后静脉血,检测血常规、凝血功能指标;取相同部位的腹主动脉、冠状动脉、肺组织标本,苏木精-伊红染色观察两组标本病理损伤变化;采用免疫组织化学染色对比两组细胞间黏附分子1的表达水平;高倍透射电子显微镜观察冠状动脉及肺组织超微结构变化。结果与结论:①常温对照组实验前、后活化部分凝血活酶时间、凝血酶原时间、血浆D-二聚体、纤维蛋白原降解产物水平及红细胞、血小板计数比较,差异无显著性意义(P>0.05);②热射病组实验后红细胞计数、活化部分凝血活酶时间、凝血酶原时间、血浆D-二聚体、纤维蛋白原降解产物水平高于实验前,且高于常温对照组;血小板计数低于实验前,且低于常温对照组,差异有显著性意义(P<0.05);③苏木精-伊红染色:常温对照组腹主动脉、冠状动脉、肺微血管组织病理结构正常;热射病组腹主动脉内皮细胞轻度水肿,未见明显异常;冠状动脉可见血栓形成、内皮细胞脱落、坏死,数量减少;肺微血管弥漫性出血、内皮细胞数量明显减少;④免疫组织化学染色结果显示:常温对照组腹主动脉、冠状动脉、肺组织观察到内皮细胞浆膜上有数量较多、呈棕黄色线状的细胞间黏附分子1阳性表达;热射病组内皮细胞浆膜上染色数量明显减少,或表达缺如,呈浅黄色的细胞间黏附分子1弱阳性表达;热射病组血管组织中细胞间黏附分子1平均吸光度值低于常温对照组(P<0.05);⑤电镜观察超微结构:热射病组冠状动脉组织可见细胞核形状不规则,线粒体肿胀;热射病组肺组织可见少量细胞核及线粒体肿胀;⑥提示热射病可导致小型猪血管内皮细胞损伤,且以微小血管损伤表现显著。     

Trophoblasts and soluble adhesion molecules in peripheral blood of women with pregnancy-induced hypertension

PROBLEM: The current hypothesis on the pathogenesis of pregnancy-induced hypertension (PIH) considers it as an endothelial disorder that is first local but with the potential of becoming general. The aim of the work was to investigate the relation of the number of trophoblast cells in maternal peripheral blood against the serum levels of soluble vascular and intercellular cell adhesion molecule (sVCAM-1 and sICAM-1) in PIH. METHOD OF STUDY: Women with PIH were at 28th to 40th week of gestation. Control group were normotensive (NT) pregnant women at 28th to 41st week of gestation. Flow cytometry was used to assess the relative number of the trophoblasts in the peripheral blood. Trophoblasts were labeled with monoclonal anti-human trophoblast protein antibody MCA 277. The presence of sVCAM-1 and sICAM-1 was determined using the enzyme-linked immunosorbent assay method. RESULTS: Women with PIH had significantly higher trophoblasts number than NT women (median 19.0, range 5.0-57.0/400 microL versus median 7.0, range 0.0-18.0/400 microL; P = 0.000011) as well as plasma level of sVCAM-1 when compared with NT women (median 730.0, range 325.0-1525.0 ng/mL versus median 493, range 310-1075 ng/mL; P = 0.02). ICAM-1 level in the PIH group was slightly elevated (median 280.0, range 174.0-524.0 ng/mL) when compared with NT women (median 260.0, range 190.0-464.0 ng/mL, P = 0.322). Eight of 21 women with PIH had proteinuria but no correlation was found between this symptom and the laboratory findings. CONCLUSION: The increased number of trophoblast cells in maternal peripheral blood and higher levels of sVCAM-1 correlate with the presence of PIH. The differences of sVCAM levels were significantly higher than those observed for sICAM. The results indicate an association between circulating trophoblasts and vascular endothelium activation, during PIH.     

人白介素10对异种内皮细胞保护作用的研究

目的：研究人白介素10(HIL-10)对活化的牛主动脉内皮细胞(BAECs)的保护作用，为HIL-10用来减轻异种排斥反应、诱导异种移植免疫耐受提供实验依据。方法：用不同浓度的HIL-10(2、5、10、20、40ng/ml)孵育BAECs2小时后，再与肿瘤坏死因子a(TNF-a，ng/ml)共孵育6小时或18小时；应用细胞-酶联免疫吸附分析方法(Cell-ELISA)检测细胞表面的E-seleetin和ICAM-1的表达。用MTT方法测定药物对细胞活性的影响。结果：用HIL-10在一定浓度内预处理BAECs后，能明显抑制TNF-a诱导的E-seleetin与ICAM-1的表达，并呈现一定的剂量依赖性。用MTT方法测定细胞活性的实验表明，各实验组细胞活性与对照组无明显差异性。结论：HIL-10能明显抑制TNF-a活化的BAECs表达Bseleetin与ICAM-1；HIL-10对BAECs有一定的保护作用。     

The role of amniotic fluid interleukin-6, and cell adhesion molecules, intercellular adhesion molecule-1 and leukocyte adhesion molecule-1, in intra-amniotic infection

PROBLEM: To determine amniotic fluid concentrations and correlations of interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and leukocyte adhesion molecule-1 (LAM-1) in patients with and without intra-amniotic infection. METHOD OF STUDY: Fourteen specimens with intra-amniotic infection and 45 without intra-amniotic infection were studied. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture. Amniotic fluid IL-6, ICAM-1, and LAM-1 levels were determined by an enzyme-linked immunoassay, and normalized by amniotic fluid creatinine levels. RESULTS: Amniotic fluid concentrations of IL-6 and LAM-1 were significantly higher in patients with than without intra-amniotic infection. However, amniotic fluid ICAM-1 concentrations were not significantly different between two groups. Amniotic fluid IL-6, LAM-1, and ICAM-1 were positively correlated. CONCLUSIONS: Our data indicate that amniotic fluid IL-6 is significantly associated with an increased adhesion molecule expression in intra-amniotic infection. However, LAM-1 plays a more important role than ICAM-1 in intra-amniotic infection.