Background &Aims: Proinflammatory interleukin (IL)-1 gene polymorphisms asso ciated with high levels of IL-1βactivity increase the risk for hypochlorhydria and distal gastric carcinoma. The aim of this study was ...Background &Aims: Proinflammatory interleukin (IL)-1 gene polymorphisms asso ciated with high levels of IL-1βactivity increase the risk for hypochlorhydria and distal gastric carcinoma. The aim of this study was to evaluate whether car riers of these polymorphic genes are protected against gastroesophageal reflux d isease (GERD). TNFA-308 polymorphisms were also studied. Methods: We prospectiv ely evaluated 385 patients without gastric cancer and peptic ulcer. Of these pat ients,383 (98 with GERD and 285 controls) were successfully genotyped for all cy tokines studied. The cagA status of Helicobacter pylori isolates was determined by polymerase chain reaction (PCR). IL1B-511/-31, IL1RN, and TNFA-308 polymor phisms were genotyped by PCR, PCR/restriction fragment length polymorphism, or PCR/confronting 2-pair primers. Histologic g astritis was assessed according to the updated Sydney system. The role of the pr oinflammatory cytokine genotypes in the genesis of GERD was evaluated before and after stratification by H. pylori status in logistic regression models controll ing for confounding factors. Results: IL1B-31 (a near-complete linkage disequi librium between polymorphism at -31 and -511 was found) and IL1RN*2 allele po lymorphisms were associated with GERD. After stratification, in the group of H. pylori-positive patients, cagA-positive status,IL1B-31 polymorphic alleles, I L1RN*2 alleles, and the degree of corpus gastritis were negatively associated w ith GERD. In the H. pylori-negative group, IL1B-31C/C genotype was inversely a ssociated with GERD even after adjustment for age and sex. Conclusions: This stu dy provides evidence supporting the independent protective role of cagA-positiv e H.pylori status and IL1B and ILRN allele polymorphisms against GERD.展开更多
文摘目的:制备针对白血病干细胞(LSC)表面标志蛋白IL1RAP(IL-1 receptor accessory protein)的特异性单克隆抗体并对其进行鉴定。方法:杂交瘤细胞3H6E10、10D8A7种植BALB/c小鼠腹腔,收获腹水,纯化后得到特异性抗人IL1RAP的单克隆抗体。分别应用非变性聚丙烯酰胺凝胶电泳(Nondenaturing-PAGE)、ELISA和Western blot法对纯化单克隆抗体分别进行抗体纯度、效价和敏感性检测。结果:获得了两种IL1RAP纯化单克隆抗体,命名为3H6E10 Mc Ab和10D8A7 Mc Ab,其纯度分别为95%和94%;两种纯化的单克隆抗体效价为1∶81000,且能特异性识别IL1RAP纯化蛋白、正常人及白血病病人的细胞内源性蛋白。结论:本研究成功制备了能特异性结合人IL1RAP的纯化单克隆抗体,为将来有效清除体内LSC提供了新途径。
文摘IL1B（Interleukin 1 beta）是一种对抗感染的前炎症因子，在肿瘤的发生发展中起着重要的作用。IL1B基因启动子区-31C／T多态性位点通过影响IL1B的转录参与癌症的发生。针对已有的研究存在结论不一致的现状，为了阐明两者之间的关系，我们对47篇发表的病例对照研究进行meta分析，其中包括11125病例和14415例对照。比值比（Odds Ratio，OR）和95％可信区间（CI）用来评估多态性位点与癌症风险的关联程度。在所有的对比中没有发现此多态性位点与所有癌症相关联。通过分层分析发现，携带C等位基因的个体比不带C等位基因的个体患肝癌的风险低（CCVS TT：OR=0．87，95％CI：0．77—0．98，Phetermgrenty=0．103；TC vs TT：OR=0．77，95％CI：0．62-0．95，Phetermgrenty=0．734；TC＋CC vs TT：OR=0．74，95％CI：0．61～0．91，Phetermgrenty=0．472）。同样，C／C基因型个体相比T，T基因型个体患胃癌风险低（OR=0．87，95％CI：0．77-0．98，Rhetermgrenty=0．103）。运用隐性模型，患胃癌的风险显著下降（OR=0．88，95％CI：0．80～0．97，Phetermgrenty=0．158），在欧洲人群（OR=0．84，95％CI：0．73-0．97,Phetermgrenty=0．070）和感染-配埘研究（OR=0．75，95％CI：0．60～0．94，Phetermgrenty=0．220）中都发现有显著下降的风险；在乳腺癌中有显著增加的风险（OR=1．34，95％CI：1．18～1．61，Phetermgrenty=0．116）。虽然一些适度偏倚不能消除，此meta分析显示IL1B-3IC基因型是癌症发生的保护因素，特别是在感染人群中。
文摘Background &Aims: Proinflammatory interleukin (IL)-1 gene polymorphisms asso ciated with high levels of IL-1βactivity increase the risk for hypochlorhydria and distal gastric carcinoma. The aim of this study was to evaluate whether car riers of these polymorphic genes are protected against gastroesophageal reflux d isease (GERD). TNFA-308 polymorphisms were also studied. Methods: We prospectiv ely evaluated 385 patients without gastric cancer and peptic ulcer. Of these pat ients,383 (98 with GERD and 285 controls) were successfully genotyped for all cy tokines studied. The cagA status of Helicobacter pylori isolates was determined by polymerase chain reaction (PCR). IL1B-511/-31, IL1RN, and TNFA-308 polymor phisms were genotyped by PCR, PCR/restriction fragment length polymorphism, or PCR/confronting 2-pair primers. Histologic g astritis was assessed according to the updated Sydney system. The role of the pr oinflammatory cytokine genotypes in the genesis of GERD was evaluated before and after stratification by H. pylori status in logistic regression models controll ing for confounding factors. Results: IL1B-31 (a near-complete linkage disequi librium between polymorphism at -31 and -511 was found) and IL1RN*2 allele po lymorphisms were associated with GERD. After stratification, in the group of H. pylori-positive patients, cagA-positive status,IL1B-31 polymorphic alleles, I L1RN*2 alleles, and the degree of corpus gastritis were negatively associated w ith GERD. In the H. pylori-negative group, IL1B-31C/C genotype was inversely a ssociated with GERD even after adjustment for age and sex. Conclusions: This stu dy provides evidence supporting the independent protective role of cagA-positiv e H.pylori status and IL1B and ILRN allele polymorphisms against GERD.
