本文選題：幽門螺桿菌 + CagA　； 參考：《廣西醫(yī)科大學(xué)》2005年碩士論文

【摘要】：目的:研究廣西南寧兒童幽門螺桿菌空泡毒素(VacA)基因和細(xì)胞毒素相關(guān)蛋白(CagA)基因的存在情況并分析各基因與胃十二指腸疾病的關(guān)系。 方法:(1) 應(yīng)用奧林巴斯GIF-XQ20 纖維胃鏡或GIF-XQ230 電子胃鏡對(duì)有上消化道癥狀的156 例兒童進(jìn)行胃鏡檢查。(2)進(jìn)行胃粘膜快速尿素酶檢測(cè)、Warthin-Starry 銀染色和HE 染色,采用PCR 方法測(cè)定胃粘膜中的Hpylori 尿素酶C 基因,并應(yīng)用間接酶聯(lián)免疫吸附法測(cè)定血清抗H.pylori-IgG,其中兩項(xiàng)結(jié)果陽性診斷為H.pylori 感染。(3)對(duì)診斷H.pylori 感染的80 例兒童的胃粘膜提取DNA,采用PCR 法對(duì)CagA 基因及VacA 基因亞型進(jìn)行分析。 結(jié)果:(1)80 例患兒胃粘膜H.pylori 菌株應(yīng)用CagA 基因的5 對(duì)引物分別擴(kuò)增CagA 基因DNA400bp、280bp、349bp、298bp 和191bp 五個(gè)片段,CagA基因的檢出率分別為43.75%、20%、55%、32.5%和61.2%,五者間差別有顯著性。(P0.01)CagA 基因總檢出率為83.7%,顯著高于單一引物擴(kuò)增的CagA 基因檢出率。輕度炎癥CagA 基因檢出率為81%,中重度炎癥CagA 基因檢出率為86.8%,差異無顯著性(P0.05)。(2)所有菌株均擴(kuò)增出VacA 基因亞型,其中s 區(qū)中s1a 檢出率為100%,s1b 和s2 未檢出,m 區(qū)中m1 檢出率為3.75%,m2 檢出率為66.25%,另有13.75%為m1、m2 均檢出,提示混合感染,而約16.25%的菌株不能用m1、m2 分型。剔除混合感染和不能用VacAm1、VacAm2 分型的病例,南寧兒童H.pyloriVacA 基因亞型有s1a/m1 和s1a/m2 兩種組合,各亞型所占比例分別為3.75%、66.25%。(3)南寧兒童的幽門螺桿菌的優(yōu)勢(shì)基因型以CagA~+、VacAs1a/m2 為主。(4)CagA 基因及VacA 基因各亞型在慢性淺表性胃炎及消化性潰瘍中的檢出率無顯著性差異(P0.05)。 結(jié)論:(1)廣西南寧兒童幽門螺桿菌以CagA~+基因?yàn)橹?單對(duì)引物中,以擴(kuò)增CagA 基因DNA191bp 片段的引物的CagA 陽性檢出率最高;增加引物對(duì)數(shù)量,可提高CagA 基因的檢出率。CagA 基因存在變異性和多態(tài)性。(2)CagA基因與胃粘膜炎癥程度無關(guān)。(3)s1a/m2 為本地區(qū)兒童幽門螺桿菌的VacA 優(yōu)勢(shì)基因型,部分患兒同時(shí)感染多株不同VacA 基因型H.pylori。(4)CagA 基因及VacA 基因各亞型均不能作為本地區(qū)H.pylori 菌株毒力強(qiáng)弱的指標(biāo)。
[Abstract]:Objective: to study the existence of Vaca gene and CagA gene in Nanning children and to analyze the relationship between Vaca gene and gastroduodenal disease. Methods: (1) 156 children with upper gastrointestinal symptoms were examined with Olympus GIF-XQ20 fibergastroscope or GIF-XQ230 electronic gastroscope. (2) Warthin-Starry silver staining and HE staining were detected by rapid urease staining in gastric mucosa. The Hpylori urease C gene in gastric mucosa was detected by PCR. Indirect enzyme-linked immunosorbent assay (Elisa) was used to detect anti-H.pylori-IgG, two of which were positive for H.pylori infection. (3) the gastric mucosal DNA was extracted from 80 children with H.pylori infection. The CagA gene and Vaca gene subtype were analyzed by PCR. Results: (1) five pairs of primers of CagA gene were used to amplify the CagA gene of H. pylori in gastric mucosa of 80 children. The detectable rates of CagA gene were 43.7575 ~ 205.55% and 61.2%, respectively. (P0.01) the total detection rate of CagA gene was 83.7, and the total detection rate of CagA gene was 83.7, which was significantly higher than that of the control group. (P0.01) the total detection rate of CagA gene was 83.7, and the detection rate of CagA gene was 83.70.The detection rate of CagA gene was 32.5% and 61.2%, respectively. (P0.01) the detection rate of CagA gene was 83.7. The detection rate of CagA gene was detected by single primer amplification. The detection rate of CagA gene was 81% in mild inflammation and 86.8% in moderate and severe inflammation (P0.05). (2). The detection rate of s1a in s1a region was 100 and that in s2 region was 3.75m2.The detection rate of M1 was 66.25m 2, and 13.75% was m1m2, indicating mixed infection, and about 16.25% strains could not be typed with m1m2. Excluding mixed infections and cases that could not be typed by VacAm1VacAm2, H.pylori Vaca gene subtypes in Nanning children were combined with s1a/m1 and s1a/m2. (3) the dominant genotype of Helicobacter pylori in Nanning children was CagA- VacAs1a / m2. (4) there was no significant difference in the detection rate of CagA gene and Vaca gene subtypes in chronic superficial gastritis and peptic ulcer (P0.05). Conclusion: (1) CagA~ gene is the dominant gene of Helicobacter pylori in Nanning, Guangxi. Among the single pairs of primers, the positive rate of CagA with the primers amplified by the 191bp fragment of CagA gene DNA was the highest, and the number of primer pairs was increased. (2) CagA gene was not related to the degree of gastric mucosal inflammation. (3) s1a/m2 was the dominant genotype of Helicobacter pylori in children. Some children were also infected with different Vaca genotypes H. pylori. (4) neither the CagA gene nor the Vaca gene subtypes could be used as an indicator of the virulence of H. pylori strains in our region.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2005
【分類號(hào)】：R346

【引證文獻(xiàn)】

相關(guān)期刊論文 前1條

1 袁章;徐艷;楊拯;龐勇;張曉;;幽門螺桿菌的致病因子致胃上皮細(xì)胞凋亡的研究進(jìn)展[J];西南軍醫(yī);2008年02期

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本文編號(hào)：2054061