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博碩士論文 etd-0827110-203936 詳細資訊
Title page for etd-0827110-203936
論文名稱
Title
黏附分子的基因多型性與川崎氏症
Genetic Polymorphisms of Adhesion Molecules and Kawasaki Disease
系所名稱
Department
畢業學年期
Year, semester
語文別
Language
學位類別
Degree
頁數
Number of pages
127
研究生
Author
指導教授
Advisor
召集委員
Convenor
口試委員
Advisory Committee
口試日期
Date of Exam
2010-07-30
繳交日期
Date of Submission
2010-08-27
關鍵字
Keywords
多型性、川崎氏症、冠狀動脈症候群、黏附分子、趨化因子
Kawasaki disease, sequelae of coronary artery, adhesion molecule, chemokine, polymorphism
統計
Statistics
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中文摘要
川崎氏症(以下簡稱川症)是一種小兒後天性心臟疾病最常見的原因,被認為是感染、免疫反應和基因感受性的合併效應,川症最嚴重之併發症為急性冠狀動脈症候群,包含心肌梗塞與冠狀動脈瘤等,目前證據顯示黏附分子與趨化因子在發炎及心血管疾病的致病方面扮演了重要角色。因此,本研究目的為評估黏附分子與趨化因子的單核苷酸多型性(P-selectin 290G>A, PSGL-1 62G>A, MCP-1 -2518A>G, SDF-1 -801G>A, PECAM-1 L125V, PECAM-1 S563N 以及 PECAM-1 R670G)與川崎氏症、第一劑丙種免疫球蛋白失效風險及冠狀動脈症候群之關聯性。總計收301位川症病童(其中185位病童不具急性或慢性的冠狀動脈症候群、81位病童僅具急性的冠狀動脈症候群及33位病童同時擁有急性和慢性的冠狀動脈症候群)與246位性別配對的健康對照孩童執行病例對照研究。此外,上述301個病童中166位川症病童的父母參與親子三元體研究。結果發現PECAM-1的三個SNPs與上述三個風險無關,但慢性冠狀動脈症候群除外。PECAM-1的Leu-Ser-Arg單套型,相較於非Leu-Ser-Arg單套型,顯著增加慢性期的冠狀動脈症候群的風險(校正勝算比是2.50,95%信賴區間為1.05-6.00,P=0.039)。以雙套型分析為基礎,我們也發現具有Leu-Ser-Arg單套型的川症病童與慢性期的冠狀動脈症候群的風險具”顯性模式”的相關性(校正勝算比是2.98,95%信賴區間為1.15-7.72,P=0.024)。此外,帶PECAM-1 Leu-Ser-Arg單套型的病童,擁有較高量的血小板(診斷後10天內的最高值)(672.6±207.6與 563.1±196.8; P=0.027)。此外,藉由PECAM-1基因型分析,我們也發現PECAM-1上的每一個單核苷酸多型性與血管中的多型核嗜中性白血球的量有關。至於其它基因的單核苷酸多型性,都與川症、第一劑丙種免疫球蛋白失效或冠狀動脈症候群後遺症風險評估無任何關聯。總而言之,PECAM-1的Leu-Ser-Arg單套型可能是川症病童發生慢性冠狀動脈症候群的遺傳標誌,然而,PECAM-1核苷酸多型性在川症病童的慢性期冠狀動脈症候群的形成過程中的角色,仍然需要進一步評估。
Abstract
Kawasaki disease (KD) is the most common cause of paediatric acquired heart disease, which may be attributed to the combined effects of infection, immunological response, and genetic susceptibility. The most severe complication in KD is acute coronary artery lesions (CALs), including myocardial infarction and coronary artery aneurysms. Mounting evidence indicates that adhesion molecules and chemokines play an important role in inflammation and cardiovascular disease on basis of pathogenesis. Thus, this study aimed to investigate the association of seven single nucleotide polymorphisms (SNPs) of adhesion molecules and chemokines (P-selectin 290G>A, PSGL-1 62G>A, MCP-1 -2518A>G, SDF-1 -801G>A, PECAM-1 L125V, PECAM-1 S563N and PECAM-1 R670G) with the risk of KD, sequelae of CALs and initial intravenous immunoglobulin (IVIG) treatment failure. A total of 301 KD children (185 without acute and chronic CALs, 81 with acute but without chronic CALs, and 33 with acute and chronic CALs) and 246 sex-matched healthy controls were recruited in the case-control study. In addition, 166 cases from the above KD children and 332 parents were recruited to carry out case-parent trio study. We found that PECAM-1 3 SNPs polymorphisms were not associated with above several risks, except for CALs in chronic stage. As compared with non-Leu-Ser-Arg haplotype, Leu-Ser-Arg haplotype was associated with a significant increased risk for CALs in the chronic stage (AOR 2.50, 95% CI 1.05-6.00, P=0.039). Analyses based on the diplotypes of PECAM-1 also showed that Leu-Ser-Arg allele had a significant increased risk of CALs in chronic stage in dominant manner (AOR 2.98, 95% CI 1.15-7.72, P=0.024). In addition, carriers of Leu-Ser-Arg allele had significant increased counts of platelet (×1000/Cumm) (672.6±207.6 versus 563.1±196.8; P=0.027) within 10 days of diagnosis of KD. Moreover, we also found a significant correlation between each SNP and polymorphonuclear neutrophil counts by genotype analysis. As for other genes, there were no markedly different outcomes regardless of the risk of KD, sequelae of CALs or initial IVIG treatment failure. In conclusion, the haplotype Leu-Ser-Arg of PECAM-1 is a genetic marker of susceptibility to sequelae of chronic CALs for KD patients. However, the role of PECAM-1 SNPs in CALs formation in the chronic stage in KD patients still needs further evaluation.
目次 Table of Contents
Abbreviations --------------------------------------------------------------------------------------------5
Abstract in Chinese -------------------------------------------------------------------------------------7
Abstract in English --------------------------------------------------------------------------------------8
Contents --------------------------------------------------------------------------------------------------10
Introduction
1. Kawasaki disease ----------------------------------------------------------------------------11
2. Epidemiology ---------------------------------------------------------------------------------11
3. Coronary artery lesions and basic pathogenesis of the arterial remodeling ----------12
4. Microbes of Kawasaki disease -------------------------------------------------------------14
5. Inflammation, adhesion molecules and transendothelial migration -------------------14
6. References -------------------------------------------------------------------------------------25
Specific Aims --------------------------------------------------------------------------------------------35
Subjects and Methods ----------------------------------------------------------------------------------37
Results
1. KD risk ----------------------------------------------------------------------------------------43
2. The risk of initial IVIG treatment failure--------------------------------------------------47
3. The risk of CALs in the acute and chronic stage-----------------------------------------50
4. The relationship between each gene SNP and clinical laboratory findings-----------55
Discussion
1. PECAM-1 -----------------------------------------------------------------------------------57
2. P-selectin and PSGL-1 --------------------------------------------------------------------66
3. Chemokines ---------------------------------------------------------------------------------68
4. With regard to genetic epidemiological study and study limitations ---------------70
Conclusioin ---------------------------------------------------------------------------------------------71
5. References --------------------------------------------------------------------------------- 71
Figures ---------------------------------------------------------------------------------------------------79
Tables ----------------------------------------------------------------------------------------------------88
Appendix I
1. Preliminary data
1-1 The relationship with oxidative stress and Kawasaki disease ---------------------119
1-2 Tables -------------------------------------------------------------------------------------122
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Wittchen, E.S. (2009). Endothelial signaling in paracellular and transcellular leukocyte transmigration. Front Biosci 14, 2522-2545.

Woodfin, A., Voisin, M.B., and Nourshargh, S. (2007). PECAM-1: a multi-functional molecule in inflammation and vascular biology. Arterioscler Thromb Vasc Biol 27, 2514-2523.

Yan, H.C., Pilewski, J.M., Zhang, Q., DeLisser, H.M., Romer, L., and Albelda, S.M. (1995). Localization of multiple functional domains on human PECAM-1 (CD31) by monoclonal antibody epitope mapping. Cell Adhes Commun 3, 45-66.

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