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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 伍安怡(Betty A. Wu-Hsieh) | |
| dc.contributor.author | Yang-Ding Lin | en |
| dc.contributor.author | 林洋鼎 | zh_TW |
| dc.date.accessioned | 2021-06-12T18:15:57Z | - |
| dc.date.available | 2012-09-13 | |
| dc.date.copyright | 2007-09-13 | |
| dc.date.issued | 2007 | |
| dc.date.submitted | 2007-08-29 | |
| dc.identifier.citation | Reference List
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/27695 | - |
| dc.description.abstract | 登革病毒感染會造成嚴重的登革出血熱與登革休克症候群，然而其致病機制仍不清楚。最近的研究顯示內皮細胞可能是登革病毒的宿主細胞而且可能產生血管病變。利用登革出血小鼠動物模式的研究結果提供了證據支持內皮細胞受損在登革出血熱的致病機轉扮演關鍵角色。本研究以不同劑量的第二型登革病毒16681病毒株，利用真皮間注射方式感染免疫健全的C57BL/6小鼠。當給予小鼠2 × 109、4 × 108以及 4 × 107 PFU的病毒感染後，在三天後會分別造成81.8%、54.5%以及36.3% 的病毒感染小鼠全身性的出血；而給予小鼠4 × 106 PFU的病毒感染，則沒有病毒感染小鼠有出血的現象。利用流氏細胞儀器分析顯示出血小鼠的周邊血循環內皮細胞(CEC)數量增多。此外，出血小鼠的血小板的數量有顯著降低的情形。免疫螢光染色結果顯示於病毒感染小鼠出血的皮下組織中血管的內皮細胞會表現誘導型一氧化氮生成酵素(iNOS)和硝基化酪氨酸(nitrotyrosine)，此結果顯示由大量產生之一氧化氮及活性氧分子所導致的氧化壓力可能參與在與血管內皮受損。為了釐清一氧化氮及活性氧分子是否參與登革病毒所引發的出血，以NADPH-oxidase抑制劑餵食一氧化氮缺陷小鼠。結果顯示在一氧化氮缺陷小鼠或抑制活性氧分子可使受2 × 109 PFU登革病毒感染小鼠的出血率下降(分別從77.8 % 降至 33.3 % 與28.6 % )。而登革病毒感染活性氧分子生成被抑制之一氧化氮缺陷小鼠後，可降低出血率以及出血的嚴重性。綜合以上研究，此研究顯示小鼠動物模式中，活性氮及活性氧分子兩者都參與在登革病毒引發出血的致病機轉。此外，此研究也顯示了循環內皮細胞數目的增加和血小板的數目減少可作為發生出血現象的指標。 | zh_TW |
| dc.description.abstract | Dengue hemorrhagic fever and dengue shock syndrome (DHF/DSS) are severe dengue disease. However, the underlying pathogenic mechanisms involved in severe dengue disease remain unclear. Recent studies demonstrated that endothelial cells (ECs) are targeted by dengue virus and vascular disorder may occur. Results from study of dengue hemorrhage mouse model provided evidence to support the possibility that EC damage is key to the pathogenesis of DHF. In the present study, immunocompetent C57BL/6 mice were inoculated with different titers of DENV sertotype 2 strain 16681 through the intradermal route. While 81.8%, 54.5%, and 36.3% of the mice receiving 2 × 109, 4 × 108, and 4 × 107 PFU DV developed hemorrhage, none of those given 4 × 106 PFU did at 3 days after infection. Flow cytometric analysis showed that mice that developed hemorrhage had numbers of circulating endothelial cells (CECs) in the peripheral blood. Furthermore, hemorrhage was accompanied by significant reduction of platelet counts. Immunofluorescence staining revealed that ECs express iNOS and nitrotyrosine in the endothelium of hemorrhage tissues, suggesting oxidative stress created by the production of high output nitric oxide and reactive oxygen species is involved in endothelium damage. To test whether nitric oxide and reactive oxygen species participate in DV-induced hemorrhage, iNOS-/- mice were treated with NADPH oxidase inhibitor. The results showed that iNOS deficiency or inhibition of ROS production reduced the percentage of mice that developed hemorrhage from 77.8 % to 33.3 and 28.6 %, respectively. Combination of iNOS deficiency and oxidase inhibitor had additive effect to reduce the severity of hemorrhage as well as the percentage of mice that developed hemorrhage. Taken together, the results of the present study demonstrate that both reactive nitrogen and oxygen species are responsible for the pathogenesis of DENV-induced hemorrhage in the mouse model. Additionally, this study also showed that high numbers of CECs and low platelet counts can be used as indicators for hemorrhage development. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-12T18:15:57Z (GMT). No. of bitstreams: 1 ntu-96-R94449006-1.pdf: 1423654 bytes, checksum: 91202827cc94d7d1eedce4e87b8c3647 (MD5) Previous issue date: 2007 | en |
| dc.description.tableofcontents | Abstract iii
Abstract (Chinese) v Chapter I Introduction - 1 - Part 1 Background - 1 - 1.1 Dengue virus and dengue - 1 - 1.2 Vascular distortion in dengue disease - 4 - 1.3 Role of reactive nitrogen and oxygen species in pathology of viral infection - 5 - 1.4 The animal models for dengue virus infection - 6 - Part 2 Rationale and Objectives - 10 - Chapter II Materials and Methods - 11 - Part 1. Experimental Procedures - 11 - 1.1 Virus - 11 - 1.2 Mice - 11 - 1.3 Intradermal infection - 12 - 1.4 Flow cytometric analysis of circulating endothelial cells (CECs). - 13 - 1.5 H & E staining. - 13 - 1.6 Platelet counts and hematocrit detection. - 14 - 1.7 Double immunofluorescence staining - 14 - 1.8 Statistical analysis - 15 - Part 2. Experimental Materials - 16 - 2.1 10X PBS buffer - 16 - 2.2 FACS staining buffer - 16 - 2.3 FACS fixation buffer - 16 - 2.4 DEPC H2O - 16 - 2.5 Reagents - 17 - 2.6 General materials - 17 - 2.7 Antibodies - 18 - 2.8 Instruments - 18 - Chapter III Results - 20 - Part 1 Dengue virus induces hemorrhage in C57BL/6 mice. - 20 - Part 2 Endothelium damage in hemorrhage mice - 21 - 2.1 Increased circulating endothelial cells in the peripheral blood of hemorrhage mice - 21 - 2.2 Hematologic findings - 22 - Part 3 Exploring the molecular mechanism of hemorrhage development in dengue virus-infected C57BL/6 mice - 23 - 3.1 The endothelial cells in hemorrhage tissues express iNOS - 23 - 3.2 Nitrotyrosine colocalizes with endothelial cells in hemorrhage tissues - 24 - 3.3 The correlation between ROS/NOS and hemorrhage development. - 24 - Chapter IV Discussion - 26 - Part 1 Alterations of vascular endothelium in dengue virus-induced hemorrhage - 26 - 1.1 Circulating endothelial cells as an indicator of vascular damage in dengue hemorrhage mouse model - 26 - 1.2 The factors involved in endothelial damage in dengue hemorrhage mouse model - 28 - Part 2 Hematologic findings in dengue hemorrhage mouse model - 29 - 2.1 Hemorrhage mice exhibit thrombocytopenia. - 29 - 2.2 Hematocrit is not different between DENV-infected and uninfected mice. - 31 - References - 34 - Figure 1. Intradermal inoculation of high dose of DV induces sytemic hemorrhage in immunocompetent mice. - 49 - Figure 2. Intradermal inoculation of DV induces hemorrhage in immunocompetent mice. - 50 - Figure 3. Increased numbers of CECs in hemorrhagic mice. - 51 - Figure 4. Hemorrhage mice exhibit thrombocytopenia. - 53 - Figure 5. Hematocrit is not different between DV-infected and uninfected mice. - 54 - Figure 6. iNOS colocalized with CD31+ endothelial cells in the subcutaneous tissues of hemorrhage mouse. - 55 - Figure 7. Nitrotyrosine colocalized with CD31+ endothelial cell in the subcutaneous tissues of hemorrhage mouse. - 57 - Table 1. Correlation between inoculation size and hemorrhage development - 59 - Table 2. Both iNOS and ROS contribute to hemorrhage development in DV-infected mice. - 60 - | |
| dc.language.iso | en | |
| dc.title | 登革出血小鼠模式中活性氮及活性氧於血管內皮之受損扮演重要角色 | zh_TW |
| dc.title | Reactive Nitrogen and Oxygen Species are Critical to Endothelium Damage in Dengue Hemorrhage Mouse Model | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 95-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 顧家綺(Chia-Chi Ku),林宜玲(Yi-Ling Lin) | |
| dc.subject.keyword | 小鼠模式,活性氮,活性氧,血管內皮, | zh_TW |
| dc.subject.keyword | Mouse Model,Reactive Nitrogen Species,Reactive Oxygen Species,Endothelium Damage, | en |
| dc.relation.page | 60 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2007-08-30 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 免疫學研究所 | zh_TW |
| 顯示於系所單位： | 免疫學研究所 | |
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| ntu-96-1.pdf 目前未授權公開取用 | 1.39 MB | Adobe PDF |
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