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1.
赵敏  陈家祺 《眼科学报》1997,13(2):70-74
目的:探讨角膜热烧伤后角膜溃烂溶解穿孔以及眼内炎症的免疫学机制。方法:在大鼠角膜上制作热烧伤模型,在烧伤后的不同阶段,制备角膜,虹膜、脉络膜巩膜复合体以及视网膜平片,采用标准的ABC免疫组化方法,观察眼局部T淋巴细胞亚群,巨噬细胞、树突细胞,MHC Ⅱ类抗原阳性细胞的动态变化。结果:烧伤后早期,角膜及虹膜即有T淋巴细胞浸润,以CD3阳性细胞为主,MHCⅡ类抗原阳性细胞也轻度增多;当角膜溶解穿孔阶段,T淋巴细胞浸润达到高峰,在T淋巴细胞亚群中,CD4明显多于CD8阳性细胞;同时,巨噬细胞、树突细胞、MHCⅡ类抗原阳性细胞也大量出现。细胞密集分布于角膜缘,在溃疡溶解处,可见MHCⅡ类抗原阳性细胞及少至中等量CD3阳性淋巴细胞。Ⅱ类抗原阳性细胞在形态学上也发生了些变化,由初期的园形变为多形性,且大小不一。当烧伤恢复期病变稳定时,各种阳性细胞逐渐减少。结论:免疫反应参与了严重角膜烧伤的发病过程,在角膜溶解穿孔的发生中起重要作用。眼科学报 1997;13:70~74。  相似文献   

2.
眼前部碱烧伤后眼内组织的前列腺素E2测定及病理学观察陈剑徐锦堂李辰眼碱烧伤后,眼前节组织角膜、虹膜、睫状体有大量炎性细胞浸润及相应的炎性损伤,尤其是角膜的病理改变被认为是导致视功能障碍的主要原因[1,2]。而眼后节是否存在炎症和组织损伤,尚未见报道。...  相似文献   

3.
家兔眼前段碱烧伤后自由基清除酶动态变化的实验研究   总被引:3,自引:0,他引:3  
家兔眼前段碱烧伤后4、24和72小时房水中自由基清除酶SOD,CAT和GSH-P_x活力均下降。提示眼前段碱烧伤存在着自由基反应的紊乱,自由基清除酶活性降低,引起角膜组织严重损伤,溃疡难以愈合。  相似文献   

4.
角膜移植排斥反应的铺片免疫组化研究   总被引:8,自引:0,他引:8  
Yang P  Gong X  Zhou H  Zhao M  Huang X  Xie C  Cao X  Jin H 《中华眼科杂志》1998,34(4):273-275,I019
目的 探讨角膜移植排斥反应的发生机制及其参与细胞的表型。方法 制备正常大鼠和穿透性角膜移植鼠的角膜和虹膜睫状体铺片,用8种单克隆抗体,于铺片上进行免疫组化染色。结果 正常周边角膜及角膜缘可见少量的T细胞(CD3)、辅助/诱导性T细胞(CD4)、抑制/细胞毒T细胞(CD8)、巨噬细胞、树突细胞、主要组织相容性复合体Ⅱ类抗原阳性细胞及β转化生长因子阳性细胞;同种角膜移植术后7及12天角膜和虹膜睫状体中  相似文献   

5.
角膜碱烧伤白细胞介素-1ra基因治疗的实验研究   总被引:1,自引:0,他引:1  
袁进  周世有  王铮  顾建军  邵应峰  黄挺  陈家祺 《眼科》2007,16(3):165-168
目的探讨阳离子聚合物包装IL-1ra重组质粒、角膜原位转染治疗角膜碱烧伤的疗效。设计实验性研究。研究对象角膜碱烧伤大鼠动物模型。方法制作Wistar大鼠角膜碱烧伤模型,随机分为2组,Ⅰ组为阴性对照(12只),结膜下注射生理盐水。Ⅱ组为IL-1ra基因治疗组(18只),以PeDNA3.1质粒作为IL-1ra基因表达载体,阳离子聚合物为转染介质,角膜基质显微注射20μg IL-1ra质粒。碱烧伤后不同时间点(3、7、21天)处死实验动物取下角膜,HE染色分析角膜组织病理变化,比较两组角膜透明性和新生血管生长情况,对角膜内浸润的炎性细胞进行计数。主要指标角膜透明性和新生血管情况,角膜组织病理变化及炎性细胞计数。结果碱烧伤造模后,对照组角膜浸润水肿明显,且随时间延长而加重,角膜基质内大量炎性细胞浸润和粗大新生血管形成。IL-1ra基因治疗组的角膜基质轻、中度水肿,角膜中性粒细胞、淋巴细胞等炎性细胞计数在不同时间点均少于对照组,角膜新生血管管径均较细。结论角膜基因原位转染可使IL-1ra在局部有效表达,抑制碱烧伤引起的角膜免疫炎症反应,为眼碱烧伤的治疗提供了新的选择。  相似文献   

6.
家兔眼前段烧伤后4、24和72小时房水中自由基清除酶SOD、CAT和GSH-Px活力的下降,提示眼前段碱烧伤存在着自由反应的紊乱,自由基清除酶活性降低,引起角膜组织严重损伤,溃疡难以愈合。  相似文献   

7.
应用环孢霉素A(简称CSA)局部滴眼,治疗严重血管化角膜行角膜移植的患者33例35眼,平均随访期21个月,其中23眼未发生排斥反应,透明成功率占65.7%。发生排斥反应的12眼,其中5眼为内皮排斥,1眼为上皮排斥,6眼为混合型排斥;经增加用药次数及结合短期内使用激素,部分病例排斥反应得以控制。用药8周后测试体内一些免疫指标较用药前有明显下降。Et-RFC,Ea-RFC值,淋巴细胞转化率,以及T-淋巴细胞亚群中的OKT3、OKT4、OKT8的值均有所下降。观察结果表明:局部应用环孢霉素A对角膜移值排斥反应的高危病例有明显的预防及治疗移植免疫排斥反应的效果。  相似文献   

8.
维生素C及葡萄糖局部与全身应用治疗眼碱烧伤   总被引:5,自引:0,他引:5  
维生素C及葡萄糖局部与全身应用治疗眼碱烧伤云南省玉溪地区人民医院眼科刘莎利,杨永福,胡亚丽,文丽仙,沈汝莲碱烧伤的损伤机制到目前为止尚不十分清楚,以往已证实,烧伤后角膜及房水中葡萄糖含量在伤后24-72小时已显著降低,至少持续1-2周[1],而动物实...  相似文献   

9.
兔角膜碱烧伤的共焦显微镜及病理观察   总被引:1,自引:1,他引:1  
汪玲  朱秀萍  吴洁  杨华  王伟 《眼科新进展》2008,28(10):740-742
目的采用角膜共焦显微镜活体动态观察兔角膜碱烧伤的病理改变,组织化学方法观察角膜组织病理学变化。方法NaOH造成兔角膜碱烧伤模型,烧伤后4d、20d、36d行角膜共焦显微镜检查及组织病理学检查。结果碱烧伤后4d,角膜即有炎性细胞浸润,出现少许CD4+、CD8+细胞;碱烧伤后20d,角膜基质中炎性细胞浸润明显,CD4+、CD8+细胞增多,瘢痕及新生血管形成;碱烧伤后36d,炎性细胞浸润减少,CD4+、CD8+细胞消失,仍可见瘢痕及新生血管。结论角膜共焦显微镜活体观察碱烧伤后角膜的创伤修复,反映角膜的病理状态,有助于指导临床治疗。  相似文献   

10.
眼前段碱性化学伤是临床上常见的致盲性眼外伤之一,对其研究多年来主要集中在眼前段,后段的研究很少。角膜重度碱烧伤后眼前节将发生一系列严重的组织病理学改变,如组织变性坏死、炎症细胞浸润等,同时角膜和房水中丙二醛(MDA)含量显著升高,超氧化物歧化酶(SOD)活性显著下降。碱烧伤后视网膜组织中是否也存在类似改变呢?我们通过建立大鼠角膜碱烧伤模型,对眼前段碱烧伤后视网膜组织的病理改变及氧自由基反应进行了初步研究,现将结果报告如下。[第一段]  相似文献   

11.
PURPOSE: The presence of antigen-presenting cells (APCs) such as Langerhans cells (LCs), an epithelial form of dendritic cells (DCs), in corneal tissue is critical for generation of immune responses, including graft rejection and herpetic keratitis. The purpose of this study was to characterize the distribution and major histocompatibility complex (MHC) antigen expression of corneal LCs. METHODS: Normal and inflamed corneas were excised from BALB/c mice, and immunofluorescence staining for CD11c, CD11b, CD45, CD80 (B7.1), CD86 (B7.2), CD3, and MHC class II (Ia) was performed by confocal microscopy on wholemount corneal epithelium. RESULTS: CD11c(+) MHC class II-positive LCs were found in the limbus and corneal periphery, but not in the center of the normal cornea. These cells were CD45 positive, exhibiting bone marrow derivation, and CD3 and CD11b negative, confirming a DC lineage. Additionally, these cells were CD80 and CD86 negative, reflecting an immature phenotype. In the central and paracentral areas, however, significant numbers of CD11c(+) LCs were detected that expressed no MHC class II. It is important to note that although the density of the LCs declined from the limbus toward the center of the cornea, they were always present. In the inflamed cornea, the expression of MHC class II and costimulatory molecules CD80 and CD86 was significantly enhanced, and present in all parts of the cornea, in contrast to the normal cornea. CONCLUSIONS: The present study demonstrates for the first time the phenotype and distribution of MHC class II-negative LCs in the murine corneal epithelium. In the inflamed cornea, the LCs become activated as reflected by expression of B7 costimulatory markers. These changes in activation markers may provide additional information for devising novel immunomodulatory strategies.  相似文献   

12.
目的:探讨内毒素全身注射所致的角膜改变。方法:使用抗单核细胞、巨噬细胞和MHC-Ⅱ类抗原阳性细胞的单克隆抗体,用标准的ABC方法于内毒素注射前、后制备的角膜平片上进行免疫组织化学染色。结果:发现在正常角膜中央区实质内有散在分布的巨噬细胞,越近角膜缘分布越密集,MHC-Ⅱ类抗原阳性细胞则仅存在于角膜缘;内毒素注射后,中央区角膜单核巨噬细胞增多,这些细胞于角膜实质内发生了一系列形态学改变,MHC-Ⅱ类抗原阳性细胞仅见于注射后早期的中央区角膜内皮面。结论:内毒素诱导的角膜中巨噬细胞的增多可能是机体应激状态下的重要防御机制,角膜实质中MHC-Ⅱ类抗原的缺如则对维持角膜局部免疫微环境的稳定性有重要意义。眼科学报1996;12:70—74。  相似文献   

13.
顾宏卫  胡楠 《国际眼科杂志》2013,13(6):1093-1095
目的:探索相对稳定性强、一致性好的大鼠角膜碱烧伤动物模型。方法:将87只SD大鼠分为角膜缘碱烧伤20s组(A组,34只),角膜缘碱烧伤40s组(B组,23只),角膜中央碱烧伤40s组(C组,30只),用浸润1mol/L氢氧化钠的滤纸片,分别烧灼大鼠角膜缘和角膜中央,术后7d裂隙灯显微镜观察角膜透明度、角膜溃疡及角膜新生血管情况,并记录上述指标。结果:角膜缘碱烧伤(B组)较角膜中央烧伤(C组)溃疡发生率、角膜穿孔率和角膜上皮荧光素钠染色阳性率高,且有统计学差异(P<0.05);角膜缘烧灼时间长组(B组)溃疡发生率及角膜穿孔率高于角膜缘烧灼时间短组(A组),且有统计学差异(P<0.05);烧灼角膜缘和角膜中央(A,B,C组)均能诱导出角膜新生血管。结论:对于研究角膜新生血管的动物模型,以选择3mm圆形滤纸片角膜中央烧伤为佳;对于研究角膜缘干细胞缺乏所致角膜病变的实验,以选择环形滤纸片放置于角膜缘20s为佳。  相似文献   

14.
AIM: To investigate the infiltration and activation of lymphocyte in iris-ciliary body and anterior chamber after allogenic penetrating keratoplasty (PK), for further revealing the role of iris-ciliary body in corneal allograft immune rejection. METHODS: In the mice models of PK, BALB/C mice received orthotopic isografts (n =35) or C57BL/6 donor allografts (n =25). Grafts were examined daily for 3 weeks by slit-lamp microscopy and scored for opacity. The infiltration of CD4+ T lymphocyte in iris-ciliary body and anterior chamber was examined by immunohistology and the mRNA of CD80 and CD86 in both cornea graft and iris-ciliary body by RT-PCR was analyzed in allograft recipient at days 3, 6, 10 and the day when graft rejection occurred. Isograft recipients were examined as control at the corresponding time points. Transmission electron microscope was used to study the ultrastructure, especially cell infiltration, of iris-cilary body and corneal graft at day 3, 7 and the day when rejection occurred after allogenic PK. RESULTS: Rejection was observed in all the allograft recipients followed more than 10 days, at a median time of 15 days (range 12-18 days), but not in any of isografts. CD4+ T cells were first detected at day 6 after transplantation in limbus and Ciliary body, and then in the stroma of recipient, iris, anterior chamber and corneal allograft with an increased number until graft rejection occurred. CD80 and CD86 mRNA were detected under RT-PCR examination in both graft and iris-ciliary body of allograft recipient, but not in any of isograft recipient. Three days after operation, lymphocytes and monocytes macrophages were visible in iris blood vessels and the anterior chamber, and vascular endothelial cell proliferation and activation were significant under transmission electron microscopy examination. At day 7, corneal endothelial cells became thinner. Lymphocytes and mononuclear macrophages were found with great number in the anterior chamber and adhered to the corneal endothelium. Blood vessels in iris increased and were filled with lymphocytes. And lymphocytes were detected to migrate through endothelial cell gap out of vessels. When allograft rejection occurred, macrophages attached to endothelial cells with large number of lymphocytes and macrophages infiltrating in iris. CONCLUSION: Lymphocyte infiltration and activation occurred in iris-ciliary body after allogenic PK, and the lymphocytes could migrate from iris blood vessel to the anterior chamber, which might play an important role in corneal allograft immune rejection.  相似文献   

15.
Purpose To investigate the morphological changes in the cornea during the development of experimental immune-mediated blepharoconjunctivitis (EC).Methods EC was induced in Brown Norway (BN) rats by active immunization with ovalbumin (OVA) emulsified in complete Freunds adjuvant and a subsequent challenge by OVA eyedrops. The corneas were analyzed immunohistochemically.Results Before the induction of EC, cells stained with OX6 (rat MHC class 2, RT1B), ED1 (tissue macrophages), ED2 (resident macrophages), CD4, or major basic protein were present in the peripheral corneal stroma. ED1- and OX6-stained cells were also observed in the central corneal stroma, and their number increased after the antigen challenge. Infiltration of cells stained with ED1, ED2, OX62 (dendritic cells), CD4, or CD3 (T cells) from the limbus to the peripheral corneal stroma started 6h after the antigen challenge. Expression of MHC class 2 molecules was induced on the corneal epithelium by the antigen challenge.Conclusions The present study demonstrates for the first time the phenotypic changes and distribution of inflammatory cells in the cornea during the development of EC. Jpn J Ophthalmol 2004;48:333–339 © Japanese Ophthalmological Society 2004  相似文献   

16.
PURPOSE: Macrophages and dendritic cells (DC) are considered to play an important role in the initiation and propagation of uveitis. Little is known about these cells in the normal pig uveal tract, despite the fact that the pig eye shares many similarities with the human eye and is considered as a suitable species to investigate the pathogenesis of human ocular disease. The aim of this study was to investigate the presence of immunocompetent cells in the uveal tract of the normal pig. METHODS: Iris and choroid wholemounts and cryostat sections were obtained from normal pig eyes. Single and double immunohistochemistry was performed by using anti-porcine leukocyte (CD45), anti-porcine macrophage (CD163, CD14), anti-porcine MHC class II (MCA1335), anti-human MHC class II (MCA379G), anti-porcine B lymphocyte (IgM), anti-porcine T lymphocyte (CD6) and anti-porcine granulocyte (MCA1219) monoclonal antibodies. RESULTS: A rich network of dendritiform CD163 positive tissue macrophages was observed in normal pig iris and choroid wholemounts (368 + 84/mm(2), 402 + 97/mm(2), respectively). Approximately 50% of the CD163 positive tissue macrophages in the iris coexpressed MHC class II. Double immunostaining revealed that a small population of the MHC class II positive cells, did not express macrophage markers, and probably represent classical DCs. B lymphocytes and granulocytes were not detected in iris and choroid wholemounts. An occasional T cell could be observed per high power field in iris wholemounts but not in the choroid. CONCLUSIONS: The present study reveals that the normal pig uveal tract contains a rich network of tissue macrophages and MHC class II positive dendritiform cells. At least three populations could be distinguished: MHC class II positive and negative tissue macrophages and MHC class II+ dendritiform cells lacking tissue macrophage markers.  相似文献   

17.
基质金属蛋白酶抑制剂治疗碱烧伤后兔角膜融解的研究   总被引:6,自引:0,他引:6  
Liu H  Zhang W  Pan Z  Wu Y 《中华眼科杂志》2002,38(9):539-542
目的研究基质金属蛋白酶抑制剂(GM 6001)在治疗兔角膜碱烧伤后角膜融解中的作用.方法将28只兔随机分为A、B组,将浸有2 mol/L(16只)及1 mol/L(12只)氢氧化钠的滤纸片分别置于A、B组兔右眼角膜上制备角膜重和中度碱烧伤模型;每组均设治疗和对照组,A、B治疗组术眼分别滴浓度为400及200 mg/L的GM 6001滴眼液,对照组滴药物基质液;均治疗30 d,然后处死动物.观察其角膜融解及混浊等情况,并进行病理组织学检查.结果 A组对照组8只兔眼角膜自伤后(13±5) d开始全部发生融解,2只兔眼发生角膜穿孔;治疗组,仅有2只兔眼烧伤后(19±4) d发生角膜融解,无角膜穿孔;两组角膜融解发生率及角膜穿孔率比较,差异有显著意义(P<0.05).治疗组角膜融解开始的时间亦明显迟于对照组(P<0.05).B组对照组6只兔角膜自伤后(14±6) d全部融解,1只兔眼角膜穿孔;治疗组2只兔眼角膜自伤后(19±4) d融解,无角膜穿孔;两组角膜融解发生率间比较,差异有显著意义(P<0.05);治疗组角膜混浊程度明显低于对照组(P<0.01).病理检查结果显示治疗组角膜胶原纤维破坏轻,炎性细胞浸润明显少于对照组.结论 GM 6001可抑制和延迟碱烧伤后角膜融解的发生和发展,降低角膜胶原纤维的破坏及角膜组织中炎性细胞的浸润.  相似文献   

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