小鼠孕早期子宫内膜ICAM-1 mRNA的表达及调节

目的：为探讨细胞间粘附分子－１ｍＲＮＡ（ＩＣＡＭ－１）在孕早期的作用和细胞因子对其表达的影响。方法：用ＲＴ－ＰＣＲ法测定孕１～８ｄ小鼠子宫内膜ＩＣＡＭ－１的表达；在小鼠孕２～４ｄ分别腹腔注射细胞因子ＬＩＦ、ＩＬ－１β或ＩＬ－１ｒａ，测定并比较各组孕第４天子宫内膜ＩＣＡＭ－１ｍＲＮＡ表达水平。结果：ＩＣＡＭ－１ｍＲＮＡ孕第１天表达量较低，第２天开始升高，第４天达高峰（Ｐ〈０．０１）。此后缓慢下降。与对照组相比。ＬＩＦ和ＩＬ－１β组ＩＣＡＭ－１ｍＲＮＡ的表达水平升高（Ｐ〈０．０１）。结论：ＩＣＡＭ－１在着床期表达水平较高，可能参与了着床过程中的胚胎粘附。细胞因子ＬＩＦ和ＩＬ－１可能是子宫内膜表达ＩＣＡＭ－１的潜在促调节因子。     

粘附分子对CD3介导的胸腺细胞[Ca^2＋]i应答的影响

ＬＦＡ－１和ＩＣＡＭ－１广泛表达于各胸腺细胞亚群，但ＩＣＡＭ－１在ＰＮＡ￣＋细胞的表达下调。本文报道：用抗ＬＦＡ－１／ＩＣＡＭ－１和抗ＣＤ３单抗，分析了粘附分子ＬＦＡ－１／ＩＣＡＭ－１对抗ＣＤ３诱导的胸腺细胞［Ｃａ￣（２＋）］ｉ应答的影响。结果显示，可溶性抗ＬＦＡ－１／ＩＣＡＭ－１可抑制ＣｏｎＡ刺激的胸腺细胞增殖，且以抗ＬＦＡ－１抗体的作用更为显著，在ＣｏｎＡ或抗ＣＤ３诱导的胸腺细胞［Ｃａ￣（２＋）］ｉ应答中，抗ＬＦＡ－１单抗可明显抑制［Ｃａ￣（２＋）ｉ升高。但如果用二抗交联ＣＤ３和ＬＦＡ－１，胸腺细胞［Ｃａ￣（２＋）ｉ则显著高于单独交联ＣＤ３时的水平（Ｐ＜０．０１），而ＣＤ３与ＩＣＡＭ－ｌ交联却无此效应，此外，仅交联ＬＦＡ－１或ＩＣＡＭ－１也无诱导［Ｃａ￣（２＋）］ｉ应答的作用。提示在ＬＦＡ－ｌ与ＩＣＡＭ－１介导的胸腺细胞与胸腺基质细胞相互作用中，ＬＦＡ－１可为ＴＣＲ／ＣＤ３途径介导的胸腺细胞活化提供复合刺激信号。     

系统性红斑狼疮患者B淋巴细胞EBV-LMP1和ZEBRA的表达研究

目的：探讨ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ在系统性红斑狼疮患者（ＳＬＥ）的表达情况。方法：间接荧光免疫标记，流式细胞仪检测。结果：ＳＬＥ患者Ｂ淋巴细胞中ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ的表达显著高于正常对照组（Ｐ＜０．０１）。活动期患者ＣＤ２３＋细胞ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ的表达率均高于ＣＤ１９＋细胞（Ｐ＜０．０１）。非活动期患者ＣＤ２３＋细胞ＥＢＶ－ＬＭＰ１表达也高于ＣＤ１９＋细胞（Ｐ＜０．０１）。但ＥＢＶ－ＺＥＢＲＡ表达在两亚群间差异没有统计学意义（Ｐ＞０．０５）。结论：朋病毒参与了ＳＬＥ的发病机制，病毒主要以潜伏期状态存在于患者中，病毒复制促进病情发展，检测Ｂ淋巴细胞ＥＢＶ－ＬＭＰ１和ＺＥＢＲＡ的表达率，有助于病情活动指标的判断。     

B7/CD28和ICAM-1/LFA-1共刺激信号对T及B细胞功能影响的研究

目的　研究共刺激途径Ｂ７／ＣＤ２８ 和ＩＣＡＭ１／ＬＦＡ１ 对Ｔ 细胞活化以及Ｂ 细胞效应的作用。方法　在体外建立ＡＰＣＴＢ 细胞反应系统, 用Ｂ７１ 单抗和ＩＣＡＭ１ 单抗分别阻断Ｂ７／ＣＤ２８ 和ＩＣＡＭ１／ＬＦＡ１ 共刺激途径, 利用３ ＨＴｄＲ 法检测Ｔ 细胞增殖,ＥＬＩＳＡ 法测定Ｂ 细胞分泌的抗体, 用ＲＴＰＣＲ 法检测细胞因子基因的表达。结果　Ｂ７１ 单抗和ＩＣＡＭ１ 单抗均可抑制Ｔ 细胞增殖及ＩＬ２ 的产生。Ｂ７１ 单抗可下调Ｂ 细胞抗体的产生（ Ｐ＜ ０ ．０５） , 而ＩＣＡＭ１ 单抗未见明显的抑制（ Ｐ＞ ０ ．０５） 。Ｂ７１ 单抗和ＣｓＡ 联用能阻断Ｔ 细胞增殖活性及Ｂ 细胞的效应, 而ＩＣＡＭ１ 单抗和ＣｓＡ联用则无此作用。Ｂ７１ 单抗能下调ＩＬ２ 和ＩＦＮγｍ ＲＮＡ 表达,Ｂ７１ 单抗和ＣｓＡ 联用则阻断ＩＬ２ 和ＩＦＮγｍ ＲＮＡ 表达,ＩＬ４ 和ＩＬ１０ ｍ ＲＮＡ 仍可表达。结论　Ｂ７／ＣＤ２８ 和ＩＣＡＭ１／ＬＦＡ１ 共刺激途径在Ｔ 细胞活化中具有不同的作用,Ｂ７１ 单抗和ＣｓＡ 联用可导致Ｔ 细胞功能失活即无能。     

腮腺淋巴上皮瘤样癌与EB病毒感染的关系

目的：研究ＥｐｓｔｅｉｎＢａｒｒ 病毒（ＥＢＶ）与腮腺淋巴上皮瘤样癌（ｌｙｍｐｈｏｅｐｉｔｈｅｌｉｏｍａｌｉｋｅｃａｒｃｉｎｏｍａ,ＬＥＬＣ）的关系,并检测瘤细胞内ＥＢＶ 基因编码产物。方法：作者收集了中山医科大学所属病理科１９８６ 年１ 月至１９９５ 年１２ 月间３２ 例腮腺ＬＥＬＣｓ．。３２ 例ＬＥＬＣ石蜡包埋标本再次切片。采用免疫组化和原位核酸杂交法检测瘤细胞内ＥＢＶ 基因表达产物。结果：（１） 在１２５例腮腺癌中有３２ 例淋巴上皮瘤样癌,占总病例的２５－６％ （３２／１２５） 。（２）所有３２ 例腮腺ＬＥＬＣ组织中均有数量不等的ＥＢＮＡ１ 和ＥＢＥＲｓ 阳性瘤细胞。（３）２７ 例ＬＥＬＣ 组织中部分瘤细胞表达ＬＭＰ１ 。（４） 所有标本中均未见ＺＥＢＲＡ 阳性细胞。（５）３２例腮腺ＬＥＬＣ组织中ＥＡＤ、ＶＣＡ和ＭＡ的阳性表达率分别为７１－９ ％（２３／３２） 、６８－８ ％（２２／３２） 和１２－５％ （４／３２） 。结论：（１） 在鼻咽癌高发的广州地区,腮腺ＬＥＬＣ的发病率也较高。（２）腮腺ＬＥＬＣ 组织中均有ＥＢ病毒感染。（３）ＥＢ病毒在腮腺ＬＥＬＣ的感染主要为潜伏Ⅱ型,即表达ＥＢＮＡ１ 、ＥＢＥＲｓ 和ＬＭＰ１     

肠道T细胞淋巴瘤中的EB病毒感染和T细胞内抗原1的表达

目的 探讨ＥＢ病毒感染在肠道Ｔ细胞淋巴瘤发病中的意义。方法 用ＥＢＥＲ１／２原位杂交及三步ＡＢＣ法免疫组织化学染色技术,观察２４例肠道Ｔ淋巴瘤患者中ＥＢ病毒感染及Ｑ细胞内抗原（ＴＩＡ－１）抗原表达情况,选用的抗体有ＴＬＡ－１,ＬＭＰ－１,ＣＤ３,ＣＤ２０,ＣＤ３０和ＣＤ４５ＲＯ等。     

Epstein—Barr病毒潜伏膜蛋白2A重组痘苗病毒转染DC及特异性CTL的体外诱导

通过ＥＢ病毒ＬＭＰ２Ａ重组痘苗病毒转染的ＤＣＳ体外诱导ＬＭＰ２Ａ特异性ＣＴＬ,并通过ＧＭ－ＣＳＦ、ＩＬ－４和ＴＮＦ－ａ培养体系,我们诱导出了人外周血单核细胞来源的ＤＣ。同时选用在鼻咽癌患者中表达的ＥＢ病毒潜伏蛋白之一ＬＭＰ２Ａ作为靶基因,利用重组痘苗病毒转染诱导的ＤＣＳ。ＤＣＳ与自体ＰＢＭＣＳ混合培养,在ＩＬ－２的刺激作用下获得特异性ＣＴＬ。结果如下：１．人外周血单核细胞经ＧＭ－ＣＳＦ、ＩＬ－４、ＴＮＦ－ａ的混合培养,１０天可获得成熟的功能性ＤＣＳ。ＦＡＣＳ检测显示ＤＣ表面相对特异性标志ＣＤ８３…     

促炎症细胞因子刺激人类关节骨膜Ｂ型细胞表达粘附分子

目的：透析相关性淀粉样变（ＤＲＡ）病人关节滑膜组织粘附分子表达增强,并与局部炎与细胞浸润密切相关。旨在探讨ＤＲＡ时秀导滑膜细胞分子表达上调的机制,方法：分离正常人关节滑膜Ｂ型细胞,与晚期糖基化终产物修饰的β微球蛋白（ＡＧＥ－β２m）、天然β２m、肿瘤坏死因子－α（ＴＮＦ－α）,白细胞介素－１β（ＩＬ－１β）在体外共同培养,用荧光单克隆抗体染色,流式细胞仪检测定量分析滑膜Ｂ型细胞表面细胞间粘附分子－１（ＩＣＡＭ－１）,血管细胞间粘附分子－１（ＶＣＡＭ－１）、Ｅ－选择素（Ｅ－selectin)的表达,结果：正常关节滑膜Ｂ型细胞表达ＩＣＡＭ－１、ＶＣＡＭ－１,但不表达Ｅ－selectin.IL-1β、ＴＮＦ－α能以时间和剂量依赖的方式上调滑膜Ｂ型细胞ＩＣＡＭ－１、ＶＣＡＭ－１的表达,但无诱导Ｅ－selectin表达的作用。ＡＧＥ－β２m 和β２m对Ｂ型细胞粘附分子的表达无直接影响,结论：ＤＲＡ时关节组织存在的促炎症细胞因子可能上调滑膜细胞粘附分子的表达,从而促使局部的单核细胞浸润。     

B7／CD28和ICAM—1／LFA—1共刺激信号对T及B细胞功？…

目的 研究共刺激途径Ｂ７／ＣＤ２８和ＩＣＡＭ－１／ＬＦＡ－１对Ｔ细胞活化以及Ｂ细胞效应的作用。方法 在体外建立ＡＰＣ：Ｔ：Ｂ细胞反应系统,用Ｂ７－１单抗和ＩＣＡＭ－１单抗分别阻断Ｂ７／ＣＤ２８和ＩＣＡＭ－１／ＬＦＡ－１共刺激途径,利用＾３Ｈ－ＴｄＲ法检测Ｔ细胞增殖,ＥＬＩＳＡ法测定Ｂ细胞分泌的杭体,用ＲＴ－ＰＣＲ法检测细胞因子基因的表达。结果 Ｂ７－１单抗和ＩＣＡＭ－１单坑均可抑制Ｔ细胞增殖及ＩＬ     

锌对大鼠免疫器官细胞周期增殖特性分析

本文通过建立大鼠缺锌（ＺＤ）、高锌（ＺＥ）模型检测锌对骨髓、胸腺、脾脏细胞周期的影响。结果表明：（１）ＺＤ、ＺＥ组的骨髓、胸腺、脾脏细胞周期，以及脾Ｔ、Ｂ淋巴细胞的Ｇ·／Ｇ１期细胞增多，而Ｓ期、Ｇ２＋Ｍ期细胞减少、与配对组（ＰＦ）、自由喂养组（ＡＬ）、缺锌补锌组（ＺＤ＋ＡＬ）间差别非常显著。（２）ＺＤ、ＺＥ组的脾脏Ｔ淋巴细胞亚群ＣＤ３·ＣＤ４非常显著低于ＰＦ、ＡＬ、ＺＤ＋ＡＬ组。ＣＤ４／ＣＤ８比值也显著下降。提示适量锌促进免疫器官细胞ＤＮＡ复利，而缺锌、高锌则抑制其细胞的增殖分化。     

Endothelial cell-matrix interactions determine maturation of dendritic cells

The fate of allo- and xenogeneic endothelial cell (EC) implants is regulated by EC-matrix interactions. While free EC are destroyed by a vigorous immune reaction, EC embedded within 3D collagen cells are well tolerated. Given the critical role DC serve in immune reactivity, we hypothesized that EC-driven DC maturation depends on EC-matrix contact. In marked contrast to DC co-cultured with a cytokine cocktail or with allo- and xenogeneic EC grown to confluence on 2D tissue culture plates, DC exposed to 3D matrix-embedded allo- and xenogeneic EC failed to mature, retaining their endocytic activity and exhibiting significantly reduced expression of maturation markers (costimulatory molecules, HLA-DR, CD83; p <0.01). Matrix-embedded EC also limited cytokine-induced maturation and activity of DC. Incubation with matrix-embedded EC inhibited DC induction of allogeneic lymphocyte proliferation (p <0.002) and EC cross-activation (ICAM-1, VCAM-1, HLA-DR, TLR2 and 4; p <0.01). The endothelium in its quiescent state is confluent and substrate adherent. The former ensures secretion of growth inhibitors rather than promoters, and the latter may ensure immune acceptance. We now demonstrate for the first time that interactions of EC with an underlying 3D matrix affect the ability of EC to drive DC maturation.     

OX-LDL诱导内皮细胞条件培养液对内皮细胞VCAM-1和ICAM-1的影响

目的探讨受损内皮细胞的自分泌和旁分泌对内皮细胞自身的影响。方法利用正常内皮细胞条件培养液和用氧化型低密度脂蛋白(OX-LDL)诱导内皮细胞的条件培养液分别作用于正常内皮细胞和受损内皮细胞,用酶联免疫细胞化学法检测血管内皮细胞黏附分子-1(VCAM-1)和细胞间黏附分子-1(ICAM-1)表达的变化。结果正常内皮细胞的条件培养液和OX-LDL诱导的内皮细胞条件培养液对正常内皮细胞VCAM-1和ICAM-1的表达作用不明显(P>0.05),而对受损内皮细胞VCAM-1和ICAM-1的表达具有明显的下调作用(P<0.01)。结论正常和受到氧化损伤的内皮细胞的自分泌和旁分泌作用对正常内皮细胞黏附分子没有影响,而对受损内皮细胞黏附分子有下调作用,说明内皮细胞可通过下调黏附分子的表达来实现自身的抗损伤作用。     

哮喘大鼠血清刺激下内皮细胞表面粘附分子ICAM—1的表达

近十五年人们才发现炎症是哮喘发病的病理基础,它以白细胞浸润为主要特征,过程由白细胞与内皮细胞表面粘附分子介导,ICAM－1就是其中之一,我们在前期活体动物实验中证实了哮喘动物肺组织中内皮细胞一白细胞粘附现象显著,并且肺组织ICAM－1高表达,这有可能是发病过程中ICAM－1大量表达于内皮细胞表面,导致内皮细胞一白细胞粘附增加的结果。本实验采用肺组织机械分离法体外培养大鼠肺内皮细胞,将哮喘病理血清与内皮细胞共同孵育,用于细胞粘附的体外研究,借助间接免疫荧光标记技术及流式细胞分离法,我们首先研究了受哮喘病理血清刺激后肺微血管内皮细胞表面ICAM－1表达的情况,结果发现,血清孵育的内皮细胞ICAM－1表达比用DMEM培养基培养的内皮细胞表达量高;哮喘血清刺激4h后ICAM－1表达量达到峰值,长于4h则很快降低;正常血清或培养基处理的内皮细胞表达持续在一个低水平。     

趋化性细胞因子MIP-1α促小鼠外周血DC前体细胞动员的实验研究

抗MIP-1α抗体可以阻断P.acnes对DC前体细胞的动员作用。对C57BL/6J(B6)小鼠静脉直接注射MIP-1α,24h后在B6小鼠外周血中F4/80-B220-CD11c+细胞明显增多,占外周血单个核细胞(PBMC)13.47%±1.4%。新鲜分离的F4/80-B220-CD11c+细胞不具有成熟DC的特征,经过细胞因子GM-CSF、IL-4和mTNF-α体外培养7d后的F4/80-B220-CD11c+细胞呈现树突状突起并形成细胞团簇,高度表达Ia、CD11c、DEC205、CD80、CD86,中度表达CD40,不表达CD8α、F4/80表面标志,并具有极强的刺激异源性T细胞增殖的能力。总之,研究表明趋化性细胞因子MIP-1α参与调节DC前体细胞的动员,并且注射MIP-1α可以直接迅速动员F4/80-B220-CD11c+DC前体细胞进入小鼠外周血。实验首次提出了用趋化性细胞因子MIP-1α动员DC前体细胞进入外周血的思路和实践,为体外获取大量功能正常的DC开辟了新的便捷途径。     

PD-L1 blockade improves immune dysfunction of spleen dendritic cells and T-cells in zymosan-induced multiple organs dysfunction syndromes

This research is to investigate the role of tolerant spleen dendritic cells (DC) in multiple organs dysfunction syndromes (MODS) at late stage. Tolerant DC and MODS were induced by intraperotineal injection of zymosan. The immunity of DC was determined by examining interleukin (IL)-10, IL-12, IL-2, major histocompatibility complex (MHC), CD86, programmed death (PD-1), programmed death ligand 1 (PD-L1), paired immunoglobulin-like receptor B (PIR-B) or T-cell proliferation in serum, spleen homogenate, DC culture or DC/T-cell co-culture. The PD-L1/PD-1 pathway was blocked using PD-L1 antibody. The IL-12p70 in serum, spleen homogenate and DC culture supernatant were decreased at 5 d and 12 d after zymosan injection while the IL-12p40 and IL-10 were increased. The expression of MHC, cluster of differentiation 86 (CD86), PD-1 and PD-L1 in spleen DCs were increased at early stage after zymosan injection. At 5 d and 12 d, the expression of MHC and CD86 was reduced while the expression of PD-1, PD-L1 and PIR-B was increased, accompanied with decreased proliferation of T-cell and decrease of IL-2 in spleen and serum. Application of PD-L1 antibody improved the above changes. At late stage of MODS mice induced by zymosan, the expression of co-stimulators and inhibitors in spleen DCs was imbalanced to form tolerant DCs which reduced the activation of T-cells. PD-L1 antibody improved the immune tolerance of DCs through intervening PD-1/PD-L1 pathway, and attenuated the inhibition of T-cell activities by tolerant DCs and the immune inhibition.     

ICAM-1、P—selectin、D—dimer在子痫前期胎盘和血浆表达研究

目的探讨细胞间黏附分子（ICAM-1）、P-选择素（P—selectin）、D二聚体（D—dimer）在子痫前期发生发展中的作用。方法随机选取子痫前期患者39例为研究组，37例正常妊娠孕妇为对照组，采用免疫组织化学技术检测两组胎盘组织中ICAM-1、P—selectin的表达情况；采用酶联免疫吸附法（ELISA）检测两组血浆ICAM-1、P—selectin和D—dimer的表达水平。结果子痫前期组胎盘ICAM-1、P—selectin的表达明显高于对照组（P〈0．05）；两组血浆均有ICAM-1、P—selectin和D—dimer的表达，子痫前期组的血浆ICAM-1、P—selectin和D—dimer表达明显高于对照组（P〈0．05）。结论子痫前期患者ICAM-1、P—selectin和D～dimer表达升高可能与子痫前期的发生发展有关，监测这些指标对病情判断及指导治疗具有重要意义。     

单纯疱疹病毒性脑炎小鼠脑组织内ICAM-1 mRNA动态变化及药物影响

目的：了解单纯疱疹病毒性脑炎(HSE)小鼠脑组织内的ICAM-1 mRNA动态变化及药物的影响。方法：采用RT—PCR方法半定量检测小鼠HSE治疗前后ICAM-1 mRNA的表达，并给予阿昔洛韦(ACV)及地塞米松(DEX)治疗，用透射电镜观察药物治疗后脑细胞结构的变化。结果：HSE小鼠在感染后第3天ICAM—1InItNAICAM-1 mRNA的表达开始增加，第4天达高蜂，第5天后逐渐下降；用药物干预的小鼠脑神经细胞改变较轻微，未找到病毒颗粒，毛细血管周围水肿减轻。结论：ICAM-1 mRNA是HSE炎症反应发生过程中的重要环节之一，HSE时早期给予ACV DEX治疗对HSE脑细胞结构有明显保护作用。     

树突状细胞在黏膜免疫模型小鼠中的分布及E-cadherin和ICAM-1表达的研究

目的通过研究小鼠树突状细胞在黏膜免疫模型小鼠中分布特征及上皮型钙黏附分子（E-cadherin）和细胞间黏附分子-1（ICAM-1）的表达,以探讨E-cadherin和ICAM-1在树突状细胞迁移过程中的调控作用.方法采用光镜和免疫组织化学染色方法,观察黏膜免疫模型小鼠中树突状细胞的分布特征;分析E-cadherin和ICAM-1的表达情况.结果体内的树突状细胞在黏膜免疫模型小鼠中,主要分布于肠系膜淋巴结、回肠集合淋巴小结、胃和空回肠黏膜及黏膜下层,与对照组相比有显著差异,其ICAM-1表达明显增高,E-cadherin表达下调,分别与对照组数密度和面密度比较有显著差异.结论在树突状细胞迁移运动过程中,E-cadherin和ICAM-1黏附分子可能起着关键性的调控作用.     

Inhibition of DC-SIGN-mediated transmission of human immunodeficiency virus type 1 by Toll-like receptor 3 signalling in breast milk macrophages

The majority of cells in early/colostrum milk are breast milk macrophages (BrMMø) expressing dendritic cell (DC)‐specific intercellular adhesion molecule 3 (ICAM3) grabbing nonintegrin (DC‐SIGN), and the expression level of DC‐SIGN on BrMMø will determine cell‐to‐cell human immunodeficiency virus type 1 (HIV‐1) transmissibility. Thus, one of the strategies to prevent vertical transmission of HIV‐1 through breast‐feeding is to find a way to suppress DC‐SIGN expression on BrMMø. As for the expression of Toll‐like receptors (TLRs) in BrMMø, TLR3 was always seen in BrMMø but not in peripheral blood monocytes (PBMo). Also, the expression of TLR3 was slightly enhanced in BrMMø when the cells were treated with interleukin (IL)‐4. Moreover, when TLR3 was stimulated with its specific ligand, the double‐stranded RNA (dsRNA) poly(I:C), DC‐SIGN expression on BrMMø was reduced even in the IL‐4‐mediated enhanced state. Some reduction may be caused by type I interferons (IFNs), such as IFN‐α/β, secreted from BrMMø. Indeed, both IFNs, particularly IFN‐β, showed a strong capacity to suppress the enhancement of DC‐SIGN expression on IL‐4‐treated BrMMø and such TLR3‐mediated DC‐SIGN suppression was partially abrogated by the addition of anti‐IFN‐α/β‐receptor‐specific antibodies. As expected, DC‐SIGN‐mediated HIV‐1 transmission to CD4‐positive cells by BrMMø was inhibited by either poly(I:C) stimulation or by treatment with type I IFNs. These findings suggest a possible strategy for preventing mother‐to‐child transmission (MTCT) of HIV‐1 via breast‐feeding through TLR3 signalling.     

Cigarette smoke extract induces expression of cell adhesion molecules in HUVEC via actin filament reorganization

Epidemiologic studies have shown a strong association between cigarette smoking and cardiovascular diseases. Various oxidative species and free radicals are produced during cigarette smoking and these lead to endothelial dysfunction and inflammation. Expression of adhesion molecules, such as intercellular adhesion molecule‐1 (ICAM‐1), E‐selectin, and vascular cell adhesion molecule‐1, and adhesion of leukocytes are present in atherosclerosis. We showed previously that a nonfractionated cigarette smoke extract (CSE) induces surface expression of ICAM‐1 and E‐selectin in human umbilical vein endothelial cells (HUVEC). We then investigated the role of the MAPKs (ERK1/2, JNK, and p38) and AP‐1 and the role of actin cytoskeleton reorganization in the CSE‐induced expression of ICAM‐1 and E‐selectin. Western blot analysis showed that CSE treatment rapidly and significantly caused phosphorylation of JNK and ERK1/2 but not of p38. Cytochalasin D (an actin filament disruptor) partially inhibited CSE‐induced ICAM‐1 and E‐selectin surface expression. However, inhibitors of ERK1/2 (PD98059) and JNK (SP600125) did not attenuate the CSE‐induced ICAM‐1 and E‐selectin surface expression. The results of electrophoretic mobility shift assay showed that CSE enhanced AP‐1 binding activity. Therefore, CSE activated AP‐1 and upregulated ICAM‐1 and E‐selectin surface expression in HUVEC seem to be via an MAPK‐independent pathway. Moreover, the dynamic reorganization of the actin cytoskeleton seems to be required for the CSE‐induced surface expression of ICAM‐1 and E‐selectin. Environ. Mol. Mutagen., 2009. © 2008 Wiley‐Liss, Inc.