玫瑰糠疹皮损血管细胞黏附分子-1的检测

目的探讨血管细胞黏附分子-1(VCAM-1)在玫瑰糠疹中的发病机制。方法采用免疫组化SP法检测玫瑰糠疹皮损血管内皮细胞VCAM-1的表达。结果皮损组血管内皮细胞VCAM-1的表达均高于正常皮肤组及玫瑰糠疹皮损周围正常皮肤组,玫瑰糠疹皮损周围正常皮肤组的表达高于正常皮肤组,差异均有显著性(P<0.05)。结论VCAM-1在玫瑰糠疹皮损血管内皮细胞上的高表达与真皮浅层血管周围淋巴细胞浸润有关,参与了玫瑰糠疹的炎症反应。     

玫瑰糠疹表皮内血管细胞黏附分子1和细胞间黏附分子1的表达

目的:研究血管细胞黏附分子(1VCAM-l)和细胞间黏附分子(1ICAM-1)在玫瑰糠疹发病中的作用。方法:采用链酶卵白素-过氧化物酶法检测表皮内VCAM-l、ICAM-1的表达。结果:VCAM-1在玫瑰糠疹皮损表皮基底层、棘层表达高于皮损周围正常皮肤及正常人皮肤,在皮损周围正常皮肤棘层表达高于正常人皮肤。ICAM-1在皮损、皮损周围正常皮肤基底层的表达高于正常人皮肤,在皮损棘层的表达高于皮损周围正常皮肤及正常人皮肤。结论:玫瑰糠疹表皮VCAM-1、ICAM-1的高表达可能与玫瑰糠疹的发病机制有关。     

Ang-1及Tie-2在寻常型银屑病皮损中的表达及其意义

目的:检测血管生成素-1(Ang-1)及其酪氨酸激酶受体-2(Tie-2)在寻常型银屑病进行期皮损和正常皮肤组织中的表达.方法:应用免疫组化方法检测24例寻常型银屑病进行期皮损和12例正常人皮肤组织Ang-1和Tie-2蛋白的表达.结果:寻常型银屑病皮损组织中,Ang-1主要表达于银屑病受累皮肤真皮乳头层的基质细胞,Tie-2主要表达于受累皮肤表皮和高度血管化的真皮乳头层的内皮细胞及真皮深层其它区域的内皮细胞;在正常皮肤组织中,Ang-1表达极弱或呈阴性表达,Tie-2仅在真皮深层内皮细胞表达.寻常型银屑病进行期皮损处的Ang-1和Tie-2受体表达明显高于正常对照组(P＜0.01),Ang-1和Tie-2的表达呈正相关(P＜0.01).结论:Ang-1通过作用于Tie-2受体,参与促进银屑病皮损处的血管生成,与银屑病血管新生密切相关.     

银屑病患者皮损及非皮损部位粘附分子免疫组化研究

目的　为了更好地了解浸润 T淋巴细胞和内皮细胞粘附分子的原位表达在银屑病皮损中的相互关系。方法　采用免疫组化染色方法研究银屑病皮损部位和非皮损部位的浸润 T淋巴细胞亚群和内皮细胞粘附分子 (ICAM- 1,EL AM- 1,VCAM- 1)的原位表达情况。结果　银屑病患者皮损部位 T细胞亚群和内皮细胞粘附分子的原位表达均显著高于非皮损部位 ,而且浸润 T淋巴细胞亚群的细胞密度和内皮细胞粘附分子的原位表达程度呈显著正相关。与正常人相比 ,银屑病非皮损部位和经外用皮质类固醇激素治疗后外观正常的皮肤内皮粘附分子仍呈上调表达。结论　银屑病患者皮肤真皮血管内皮细胞粘附分子的异常上调表达是造成银屑病复发的原因之一。     

糖皮质激素受体-α、核因子-κB、肿瘤坏死因子-α和白介素-1β在慢性皮炎中的表达

目的:探讨糖皮质激素受体(glucocorticoidreceptor,GR)-α、核因子(NF)-κB、肿瘤坏死因子(TNF)-α和白介素(IL)-1β在慢性皮炎中的表达及其意义。方法:采用SP免疫组化染色技术检测慢性皮炎与正常对照皮肤中GR-α、NF-κB、TNF-α及IL-1β的表达及其分布。结果:GR-α在慢性皮炎组与正常对照组皮肤中阳性表达的分布情况一致,GR-α不但在表皮呈弥漫性表达,还可表达于汗腺及汗管、真皮成纤维细胞、微血管内皮细胞及其周围的一些细胞成分。然而,与正常对照皮肤相比,GR-α在慢性皮炎皮损角质形成细胞及真皮血管内皮细胞的表达明显减弱。NF-κB在慢性皮炎组与正常对照组皮肤中阳性表达主要分布在表皮角质形成细胞中,在正常对照组皮肤中均为胞质表达,而在慢性皮炎组中为胞质表达和(或)胞核均有表达。TNF-α及IL-1β在慢性皮炎与正常对照皮肤角质形成细胞胞质中的表达无明显差异,为弱阳性反应。结论:慢性皮炎皮损区角质形成细胞中GR-α的表达下调有可能会影响皮损局部的抗炎机制。     

云南马齿苋提取物的抗炎机制研究

目的 探讨马齿苋提取物对肿瘤坏死因子?琢（TNF-?琢）、细胞间黏附分子1（ICAM-1）表达的影响,初步阐明马齿苋抗炎机制。方法　建立二甲苯致小鼠耳廓肿胀炎症模型,并分为4组。空白组：不采用任何干预措施,阴性对照组：建立模型后,不加干预,阳性组：模型建立后,使用韩国进口马齿苋外涂小鼠致炎处,实验组：建立模型后,使用云南马齿苋提取物涂于致炎处。组织病理及免疫组化观察TNF-?琢、ICAM-1的变化并比较各组的抗炎效果。结果　组织病理：空白组：真皮可见血管及少量淋巴细胞;阴性对照组：真皮组织疏松、水肿及大量淋巴细胞浸润;阳性组：轻度水肿,真皮血管周围可见部分炎症细胞浸润;实验组：HE染色：真皮轻度水肿,血管周围可见部分炎症细胞浸润。免疫组化：空白组：TNF-?琢、ICAM-1未见表达;阴性对照组：TNF-?琢强阳性表达于血管内皮细胞膜,ICAM-1强阳性表达于血管内皮细胞膜及淋巴细胞膜;阳性组：TNF-?琢阳性表达于血管内皮细胞膜,ICAM-1阳性表达于血管内皮细胞膜及淋巴细胞膜;实验组： TNF-?琢阳性表达于血管内皮细胞膜,ICAM-1阳性表达于血管内皮细胞膜及淋巴细胞膜。秩和检验：实验组与空白组比较TNF-?琢、ICAM-1,P值均 < 0.01,差异有统计学意义。结论　云南马齿苋抗炎机制可能与影响TNF-?琢、ICAM-1的表达有关。     

多形红斑型玫瑰糠疹1例

患者男,12岁。面部、躯干及四肢红斑脱屑伴瘙痒2个月。腹部皮损组织病理示:表皮角化过度,灶状角化不全,表皮内可见大量炎症细胞及红细胞移入,破坏正常表皮结构,真皮浅层血管和附属器周围中等量以淋巴细胞为主的炎细胞浸润,真皮乳头可见大量红细胞溢出。诊断:多形红斑型玫瑰糠疹。     

扁平苔藓皮损细胞间黏附分子-1的表达

目的: 探讨皮肤扁平苔藓皮损组织中黏附分子-1(ICAM-1)的表达及其与浸润淋巴细胞的关系.方法: 应用SP法免疫组化染色对30例扁平苔藓患者皮损组织蜡块和10例正常皮肤组织蜡块进行ICAM-1表达测定.结果: 正常表皮角质形成细胞不表达ICAM-1.76.7%(23/30)的扁平苔藓皮损处角质形成细胞表达ICAM-1.真皮内浸润淋巴细胞表达阳性.扁平苔藓皮损处角质形成细胞和真皮浸润淋巴细胞表达ICAM -1水平无统计学意义.结论: ICAM-1在扁平苔藓病理过程中可能起重要作用.     

嗜酸性粒细胞增多性皮炎患者皮损中蛋白酶活化受体2的表达及意义

目的观察蛋白酶活化受体2(PAR-2)在嗜酸性粒细胞增多性皮炎(HED)患者皮肤中的表达情况。方法采用免疫组化方法比较20例HED患者皮损及15例正常对照中PAR-2的表达情况。结果 PAR-2在皮肤的表皮全层尤其是颗粒层以及毛囊、汗腺、血管内皮细胞、神经纤维样结构中均表达。HED患者皮损真皮血管内皮细胞中PAR-2的明显表达高于正常对照(t=3.83,P0.001)。结论 PAR-2在HED患者血管内皮细胞内的表达增加,推测与其发病有一定关系。     

结缔组织疾病

20 0 4 2 30 6　系统性红斑狼疮患者皮损及外观正常皮肤核因子 κB、细胞间黏附分子 1的表达 /杨国良 (中国医科大一院皮肤科 )…… / /中华皮肤科杂志 .- 2 0 0 3,36(10 ) .- 6 0 0采用免疫组化方法检测 19例患者皮损及外观正常皮肤核因子κB(N F-κB)、细胞间黏附分子 - 1(ICAM -1)的表达 ,并设 10例正常对照。结果显示 ,1NF-κB表达 :正常人组表皮及真皮、患者外观正常皮肤组表皮细胞未见表达 ,12例真皮浸润细胞及血管表达 ;皮损组 11例表皮细胞表达 ,16例真皮浅层浸润细胞及血管表达 ,两两比较差异均有显著性 (P均 <0 .0 5)。 2 I…     

Vascular endothelial cell distribution and adhesion molecule expression in xanthoma

BACKGROUND: The migration of circulating monocytes into the dermis is considered to be essential for both the initiation and the progression of xanthoma. The contribution of vascular endothelial cells to the migration process is unclear. METHODS: Twenty cases of xanthelasma and six cases of tuberous xanthoma lesions were analyzed using immunohistochemical staining. RESULTS: Xanthoma lesions contained up to 25-fold more von Willebrand factor-stained endothelial cells than normal skin. The prevalence of E-selectin-positive endothelial cells increased by up to threefold more in xanthoma lesions than in normal skin. In contrast, the prevalence of intercellular cell adhesion molecule-1 (ICAM-1) decreased up to 3.5-fold more in xanthoma lesions than in normal skin. In xanthoma lesions, almost all ICAM-1-positive endothelial cells co-expressed with E-selectin but many endothelial cells, which only expressed E-selectin, were also found in the lesions and the ratio of macrophages to endothelial cells was higher (10:1) than that in normal skin (5:1). CONCLUSIONS: Endothelial cells proliferate and express E-selectin rather than ICAM-1 under a microenvironment in which macrophages predominate rather than endothelial cells, thereby promoting macrophage migration into xanthoma lesions.     

ICAM-1 and LFA-1 Expressions in the Lesional Skin of Annular Erythema Associated with Sjögren Syndrome

ICAM-1 and LFA-1 expression was studied in the lesional skin of ten cases of annular erythema associated with Sjögren syndrome. Most of the infiltrating mononuclear cells around blood vessels expressed LFA-1 in addition to its strong expression on vascular endothelial cells and focal expression on the epidermal basal cell layer in 3 cases. ICAM-1 expression on vascular endothelial cells was similar to LFA-1, although relatively focal and weak expression was observed on mononuclear cells. ICAM-1 expression on keratinocytes was focal and limited to the basal cell layer in annular erythema. These findings suggest that strong expression of ICAM-1 on endothelial cells but not keratinocytes and LFA-1 on mononuclear cells might play some role in the induction of skin lesions in annular erythema associated with Sjögren syndrome.     

A study of the kinetics and pattern of E-selectin, VCAM-1 and ICAM-1 expression in chronic actinic dermatitis

Summary It has been postulated that chronic actinic dermatitis (CAD), an eczematous photodermatosis. is a type IV hypersensitivity reaction. Expression of adhesion molecules on dermal blood vessels is critical to the recruitment of inflammatory cells into the skin: the pattern and kinetics of upregulation of these molecules in the skin differ following ultraviolet irradiation and delayed hypersensitivity reactions. We therefore investigated the kinetics of expression of endothelial leucocyte adhesion molecules (E-selectin) vascular-cell adhesion molecules 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) in CAD lesions induced by suberythemal solar-stimulated radiation, by immunohistochemical staining of biopsies taken at 1-168 h after irradiation. In control, unirradiated skin from CAD patients, baseline vessel-associated and interstitial ICAM-1, and vessel-associated VCAM-1 were noted; focal keratinocyte lCAM-1 expression was observed in two of the five patients. Endothelial E-selectin, and vessel-associated and interstitial VCAM-1 expression, were upregulated in induced lesions by 1-5 h in all patients, and remained elevated at 120-168 h. Vessel associated, dermal interstitial, and keratinocyte ICAM-1 expression was upregulated in all patients at 24h, and remained increased at 120-168h. These findings differ from those observed following ultraviolet irradiation of normal skin, and resemble those seen in normal skin during a delayed-type hypersensitivity reaction, supporting the hypothesis that CAD involves a type IV response to an as yet unidentified photo-induced antigen.     

Increased E-selectin, IL-8 and IL-10 gene expression in human skin after minimal trauma

While clinical observations suggest that trauma to the skin plays a critical role in the induction of skin lesions in some skin diseases, the mechanism by which these lesions are induced is not known. We have postulated that minor trauma to the skin may lead to the expression of critical adhesion molecules on epidermal endothelial cells (E-selectin) and pro-inflammatory cytokines, which would predispose these areas to the development of skin lesions. In order to test this hypothesis normal inner arm skin of 11 normal subjects was gently rubbed with a pencil eraser for 2 min. Four hours after rubbing, skin biopsies were obtained from the rubbed site and from adjacent normal, unrubbed inner arm skin. Expression of E-selectin, intercellular adhesion molecules (ICAM-1) and the mRNA of selected cytokines was studied utilizing real time polymerase chain reactions. Biopsies were also examined for the presence of an inflammatory infiltrate and for the presence of E-selectin and ICAM-1. No clinical or histologic changes were seen in the skin expression/unrubbed skin expression = 9.0; (median ratio rubbed skin expression/unrubbed skin expression range 0.9-161.0), ICAM-1 (median rubbed skin expression/unrubbed skin expression = 3.2; range 0.9-19.8), IL-8 (median rubbed skin expression/unrubbed skin expression = 6.6; range 2.6-57.3) and IL-10 (median rubbed skin expression/unrubbed skin expression = 13.1; range 2.4-29.0) was noted. Immunohistochemistry revealed the presence of E-selectin in the dermal blood vessels in three of four subjects 4 h after rubbing but not in the unrubbed skin. Changes in ICAM -1 or HLA-DR deposits were seen in the rubbed compared with the unrubbed skin. These findings demonstrated that minor trauma to skin may induce expression of E-selectin, ICAM-1 and IL-8, which may make the skin a more permissive site for the development of inflammatory reactions. These findings may play an important role in the development of skin lesions in areas of minor trauma.     

Expression of VCAM-1, ICAM-1, E-selectin, and P-selectin on endothelium in situ in patients with erythroderma, mycosis fungoides and atopic dermatitis

BACKGROUND: Erythroderma may result from different causes. At present it is unclear whether the patho-mechanisms that lead to these different types of erythroderma are identical or different. Adhesion molecules and their ligands play a major role in endothelial-leukocyte interactions, which affect the binding, transmigration and infiltration of lymphocytes and mononuclear cells during inflammation, injury, or immunological stimulation. The aim of this study was to investigate the adhesion molecule expression on endothelial cells in erythroderma in situ. METHODS: Snap-frozen skin biopsy specimens from 23 patients with erythroderma were studied. Eight had idiopathic erythroderma, 5 erythrodermic atopic dermatitis, 4 Sézary syndrome and 6 had erythroderma from miscellaneous causes. As a control we studied skin specimens from 10 patients with mycosis fungoides, 5 patients with atopic dermatitis and 5 healthy non-atopic volunteers. To determine adhesion molecule expression on endothelial cells in situ, sections were immuno-histochemically double stained with biotinylated Ulex Europaeus agglutinin 1 as a pan-endothelial cell marker, and for the adhesion molecules VCAM-1, ICAM-1, E-, and P-selectin. All double- and single-stained blood vessels in the dermis were counted. RESULTS: Mean endothelial expression in erythroderma was as follows: VCAM-1 51.4%, ICAM-1 70.1%, E-selectin 43.5%, and P-selectin 52.6%. There was no statistical difference between different groups of erythroderma. Mean expression of all adhesion molecules tested, was in Sézary syndrome higher than in mycosis fungoides albeit not significant. In erythrodermic atopic dermatitis only VCAM-1 expression was significantly higher than in lesional skin of atopic dermatitis. No differences were observed in expression of the other three adhesion molecules. CONCLUSIONS: There is no difference regarding adhesion molecule expression on endothelial cells between different types of erythroderma.     

银屑病患者血清和皮损中血管内皮细胞粘附分子的对比研究

目的 探讨银屑病患者血清和皮损中4种血管内皮粘附分子表达与银屑病疾病活动性之间的关系。方法 采用ELISA法检测36例银屑病患者治疗前后和36例健康人的血清中可溶性粘附分子（sICAM-1、sICAM-3、sVCAM-1、sELAM）的浓度。同时用ABC免疫组化染色技术检测了36例银屑病患者皮损和临床治愈处皮肤粘附分子（ICAM－1、ICAM－3、VCAM－1、ELAM）的表达情况。结果 与正常人相比，银屑病患者皮损部位4种粘附分子的原位表达呈明显上调（P＜0.005），同时患者血清中4种可溶性粘附分子浓度也明显升高（P＜0.001）。经治疗后银屑病患者皮损部位4种粘附分子的原位表达明显下调（P＜0.05），同时血清中4种可溶性粘附分子浓度比前也下降（P＜0.05）；血清中4种可溶性粘附分子的浓度与银屑病疾病活动严重指数（PASI）均呈正相关，但治疗前后sVCAM-1的水平上升和下降的幅度最大，且与PASI的相关性最好。结论 血管内皮细胞粘附分子参与银屑病的发病机制；患者血清中可溶性粘附分子浓度的升高可能与皮损部位血管内皮细胞上相应的粘附分子高表达有关；血清VCAM－1的水平可以作为反映银屑病疾病活动的一个新的敏感指标。     

Immunolocalization of adhesion molecules in psoriatic arthritis, psoriatic and normal skin

Adhesion molecule expression in synovial membrane obtained from patients with psoriatic arthritis (PA) has previously been compared with rheumatoid arthritis (RA). Although expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) was similar in both psoriatic and rheumatoid synovium, in contrast, little or no endothelial leucocyte adhesion molecule-1 (ELAM-1) was observed in psoriatic synovium. In the present study, the expression of ICAM-1. ELAM-1 and VCAM-1 was examined in the involved and uninvolved skin from patients with PA (n= 15), patients with psoriasis (Ps) but no arthritis (n= 5) and in normal skin (n= 4). ICAM-1 was intensely expressed on endothelium and keratinocytes of involved skin from patients with Ps with or without arthritis. There was constitutive expression of ICAM-1 on endothelium only in uninvolved and normal skin. In contrast, ELAM-1 expression was restricted to endothelial cells; it was widespread and intense in involved skin, but was minimal in uninvolved and normal skin. VCAM-1 was expressed on endothelium, and also on some dendritic cells in involved psoriatic skin. There was minimal VCAM-1 staining on endothelial cells in uninvolved and normal skin. In conclusion, in involved psoriatic skin from patients with and without arthritis ICAM-1, ELAM-1 and VCAM-1 expression is up-regulated on vascular endothelium, and ICAM-1 is expressed on keratinocytes. However, ELAM-1 and VCAM-1 expression seen in dermal vessels is not found in psoriatic synovial vessels. These differences suggest a mechanism for controlling cellular traffic in Ps and in PA.     

Expression of adhesion molecules and their ligands in contact allergy

Abstract Sequential biopsies from skin lesions induced by nickel sulphate and sodium lauryl sulphate, respectively, were investigated with respect to expression of extracellular matrix proteins and adhesion molecules on lymphocytes, endothelial cells, and keratinocytes. The majority of the infiltrating lymphocytes expressed VLA-4, LFA-1, CD44 and ICAM-1, a variable fraction expressed Leu-8 and VLA-5, and few or no cells were positive for VLA-1, VLA-2 and VLA-6. Noteworthy, was that the infiltrating cells showed a substantial amount of fibronectin but relatively small or negliglible presence of laminin, collagen type IV, IgG, IgA. IgM, and albumin. The fibronectin was associated with cell bodies as well as the area surrounding infiltrating cells. The number of infiltrating cells was larger in biopsies from nickel-sulphate induced lesions and the infiltrates contained more fibroneclin than biopsies from lesions induced by sodium lauryl sulphate. However, at the single-cell level, the expression of VLA antigens, LFA-1, CD44 and ICAM-1 was similar in both groups. The endothelial cells of skin biopsies from nickel-sulphate-induced lesions showed a stronger expression of VCAM-1, ELAM-1 and ICAM-I compared to biopsies from sodium lauryl sulphate-induced lesions. In the biopsies from nickel sulphate-induced lesions, the keratinocytes showed a tendency to less VLA-6 expression. These results suggest that fibroneclin plays a role in lymphocyte extravasation or extravascular lymphocyte migration.     

Fc gamma-receptors and HLA-DR antigens on endothelial cells in psoriatic skin lesions

Receptors for the Fc-part of IgG (FcR) and HLA-DR antigens on endothelial cells in normal and lesional skin from patients with psoriasis were studied in cryostat sections, using soluble immune complexes and monoclonal antibodies. FcR and HLA-DR antigens were detected on endothelial cells of dermal vessels both in sections of normal and lesional skin. The expression of FcR varied from one vessel to another and on endothelial cells within one and the same vessel. The expression of FcR and HLA-DR antigens was enhanced in sections of lesional skin compared with normal skin and most pronounced in lesional skin from active psoriasis. The enhanced expression may be mediated by interferon produced in psoriatic lesions. The presence of FcR and HLA-DR antigens on endothelial cells adds further evidence of he involvement of these cells in immune processes in the skin.