本文關(guān)鍵詞： 問(wèn)號(hào)鉤端螺旋體 黏附 內(nèi)化 細(xì)胞骨架 F-actin 磷脂酶C　出處：《浙江大學(xué)》2006年碩士論文　論文類型：學(xué)位論文

【摘要】：背景和目的 鉤端螺旋體(簡(jiǎn)稱鉤體)病是全世界流行的人獸共患病,我國(guó)也是鉤體病流行的主要疫區(qū)。鉤體通過(guò)皮膚黏膜,迅速進(jìn)入血液,并在血液和組織內(nèi)生長(zhǎng)繁殖,造成機(jī)體損傷,引起一系列癥狀和體征。其臨床綜合癥包括亞臨床感染、伴或不伴有腦膜炎的無(wú)黃疸的自限性發(fā)熱、潛在性致命的以出血、黃疸、腎衰竭為表現(xiàn)的Weil's綜合癥。鉤體在感染動(dòng)物腎臟組織內(nèi)長(zhǎng)期生存并不斷隨尿排出,提示鉤體必然具有侵入宿主細(xì)胞的能力,但確切的致病機(jī)制至今未明。 有文獻(xiàn)報(bào)道,問(wèn)號(hào)鉤體可黏附并侵入細(xì)胞,進(jìn)一步研究結(jié)果證實(shí),強(qiáng)毒力和弱毒力問(wèn)號(hào)鉤體均能侵入J774A.1及Vero細(xì)胞,前者還可侵入細(xì)胞核,而無(wú)毒力的雙曲鉤體缺乏侵入細(xì)胞的能力。近年來(lái)報(bào)道,許多致病菌黏附宿主細(xì)胞后能引起Ca~(2+)升高,Ca~(2+)可以觸發(fā)信號(hào)傳導(dǎo)機(jī)制,誘導(dǎo)宿主細(xì)胞骨架重排,最終導(dǎo)致細(xì)菌內(nèi)化入細(xì)胞。鉤體內(nèi)化細(xì)胞時(shí)能否觸發(fā)信號(hào)傳導(dǎo)機(jī)制,誘導(dǎo)宿主細(xì)胞骨架重排,尚需要研究。 在以往工作基礎(chǔ)上,本研究用微絲(F-actin)的特異性標(biāo)記物,羅丹明標(biāo)記的鬼筆環(huán)肽(Phalloidin-TRITC)染F-actin,用抗微管蛋白α亞單位的小鼠一抗(Anti-Bovine α-Tubulin,Mouse Monoclonal)和熒光素標(biāo)記的羊抗小鼠二抗(FITC-conjugated AffniPure Goat Anti-Mouse IgG)染微管(microtubule),檢測(cè)了不同毒力的鉤體侵入宿主細(xì)胞時(shí)細(xì)胞骨架的改變情況,并用磷脂酶C(PLC)信號(hào)傳導(dǎo)分子的特異性阻斷劑U73122抑制磷脂酶C信號(hào)通路,觀察其對(duì)細(xì)胞骨架改
[Abstract]:Background and objective Leptospira leptospirosis (Leptospirosis) is the most prevalent zoonosis in the world. Leptospirosis is also the main epidemic area of leptospirosis in China. Leptospirosis enters the blood rapidly through the skin mucosa. It also grows and multiplies in blood and tissue, causing damage to the body and causing a series of symptoms and signs. Its clinical syndrome includes subclinical infection, self-limited fever without jaundice with or without meningitis. Potentially fatal Weil's syndrome characterized by bleeding, jaundice, and renal failure. Leptospira survives in the kidneys of infected animals for a long time and is constantly excreted with urine. It is suggested that Leptospira must have the ability to invade host cells, but the exact pathogenetic mechanism is still unknown. It has been reported that Leptospira interrogans can adhere to and invade cells. Further studies have confirmed that both highly virulent and weakly virulent Leptospira can invade J774A.1 and Vero cells, and the former can also invade the nucleus. In recent years, it has been reported that the adhesion of many pathogenic bacteria to host cells can cause the increase of Ca~(2), which can trigger the signal transduction mechanism. Inducement of cytoskeleton rearrangement of host cells leads to bacterial internalization into cells. Whether Leptospira internalization can trigger signal transduction mechanism and induce cytoskeleton rearrangement of host cells needs to be studied. On the basis of previous work, F-actin was stained with Rhodamine labeled Phalloidin-TRITC, a specific marker of F-actinin. Anti-Bovine 偽 -Tubulin was used in mice with anti-tubulin 偽 subunit. Mouse Monoclonal) and fluorescein labeled sheep anti mouse second antibody. FITC-conjugated AffniPure Goat Anti-Mouse IgG (microtubule). The cytoskeleton changes of Leptospira with different virulence in host cells were detected, and the phospholipase C signaling pathway was inhibited by U73122, a specific inhibitor of phospholipase C (PLC) signal transduction molecule. Observation of cytoskeleton modification
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R377

【參考文獻(xiàn)】

相關(guān)期刊論文 前2條

1 王煥萍,李立偉,嚴(yán)杰,毛亞飛;問(wèn)號(hào)鉤端螺旋體內(nèi)化過(guò)程中細(xì)胞內(nèi)游離Ca~(2+)水平變化及細(xì)胞凋亡[J];中華微生物學(xué)和免疫學(xué)雜志;2005年01期

2 徐邦牢,王蓉,尹一兵,康格非;磷脂酶C信號(hào)轉(zhuǎn)導(dǎo)分子在肺炎鏈球菌觸發(fā)人肺Ⅱ型上皮細(xì)胞F-actin細(xì)胞骨架重排中的作用[J];中華檢驗(yàn)醫(yī)學(xué)雜志;2004年07期

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本文編號(hào)：1463525