AIM: To investigate the influence of IL-1B-511 gene polymorphism on IL-1B mRNA expression and gastric acid output in individual with or without Helicobacter pylori (H pylori) infection.METHODS: IL-1B mRNA expression a...AIM: To investigate the influence of IL-1B-511 gene polymorphism on IL-1B mRNA expression and gastric acid output in individual with or without Helicobacter pylori (H pylori) infection.METHODS: IL-1B mRNA expression and gastric acid secretion in 117 health volunteers were assayed using semi-quantitative RT-PCR and gastric juice assay, respectively. Pepsinogen (PG) Ⅰ and Ⅱ of 255 subjects (including 117 health volunteers) were also examined.RESULTS: T/T genotype individuals with H pylori infection had a more decreased PG Ⅰ/Ⅱ ratio. In gastric antrum mucosa, the individuals with H pylori infection had higher IL-1B expression than those without H pylori infection, but there was no obvious difference among each genotype. In gastric corpus, the individuals with H pylori infection had a significantly higher IL-1B expression than those without H pylori infection. IL-1B-511T/T genotype was markedly higher as compared with the other two genotypes. Both maximal acid output and basic acid output were similar among each genotype in IL-1B-511 gene locus, regardless of H pylori infection.CONCLUSION: IL-1B-511 T allele does not decrease gastric acid output, although it has a stimulated influence on IL-1B expression. Consequently, the pathway,through which IL-1B plays a central role in gastric cancer development, might not depend on low acid, but on the other regulation mechanisms.展开更多
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
目的对比观察电针溃疡性结肠炎大鼠上巨虚、足三里、下巨虚、阳陵泉等穴后对结肠组织白介素-1β(IL-1β)及烟碱型乙酰胆碱受体a7信使核糖核酸(nchRa7mRNA)表达的影响,探讨大肠下合穴上巨虚治疗对应腑病是否存在相对特异性。方法将70只健...目的对比观察电针溃疡性结肠炎大鼠上巨虚、足三里、下巨虚、阳陵泉等穴后对结肠组织白介素-1β(IL-1β)及烟碱型乙酰胆碱受体a7信使核糖核酸(nchRa7mRNA)表达的影响,探讨大肠下合穴上巨虚治疗对应腑病是否存在相对特异性。方法将70只健康SD大鼠随机分为空白组、模型组、上巨虚组、足三里组、下巨虚组、阳陵泉组及承筋组,每组10只,雌雄各半。除空白组外均采用2-4-6三硝基苯磺酸/乙醇溶液灌肠诱导建立大鼠溃疡性结肠炎模型,造模成功并治疗10 d后,肉眼观察大鼠结肠黏膜溃疡及炎症情况,ELISA法检测大鼠结肠组织中IL-1b含量,RT-PCR检测nAchRa7mRNA的表达。结果与模型组比,各穴位组结肠损伤有不同程度好转,组织IL-1β含量明显偏低而n ACh Ra7m RNA表达均较高(P<0.05,P<0.01),且上巨虚组、足三里组结肠溃疡评分亦较低(P<0.05,P<0.01);与上巨虚组比,其他4个穴位组结肠n AChRa7mRNA表达均较低(P<0.01),而下巨虚组、阳陵泉组、承筋组结肠溃疡及炎症损伤较严重,结肠溃疡评分及IL-1b含量均偏高(P<0.05,P<0.01)。结论电针治疗溃疡性结肠炎的机制可能是通过影响IL-1β、n Ach Ra7m RNA等调节异常的免疫功能,改善结肠黏膜损伤等来实现的;上巨虚治疗溃疡性结肠炎的总体效应优于足三里、下巨虚、阳陵泉及承筋穴,说明上巨虚穴与对应大肠腑之间存在一定的相对特异性。展开更多
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AIM: To investigate the influence of IL-1B-511 gene polymorphism on IL-1B mRNA expression and gastric acid output in individual with or without Helicobacter pylori (H pylori) infection.METHODS: IL-1B mRNA expression and gastric acid secretion in 117 health volunteers were assayed using semi-quantitative RT-PCR and gastric juice assay, respectively. Pepsinogen (PG) Ⅰ and Ⅱ of 255 subjects (including 117 health volunteers) were also examined.RESULTS: T/T genotype individuals with H pylori infection had a more decreased PG Ⅰ/Ⅱ ratio. In gastric antrum mucosa, the individuals with H pylori infection had higher IL-1B expression than those without H pylori infection, but there was no obvious difference among each genotype. In gastric corpus, the individuals with H pylori infection had a significantly higher IL-1B expression than those without H pylori infection. IL-1B-511T/T genotype was markedly higher as compared with the other two genotypes. Both maximal acid output and basic acid output were similar among each genotype in IL-1B-511 gene locus, regardless of H pylori infection.CONCLUSION: IL-1B-511 T allele does not decrease gastric acid output, although it has a stimulated influence on IL-1B expression. Consequently, the pathway,through which IL-1B plays a central role in gastric cancer development, might not depend on low acid, but on the other regulation mechanisms.
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.
文摘目的对比观察电针溃疡性结肠炎大鼠上巨虚、足三里、下巨虚、阳陵泉等穴后对结肠组织白介素-1β(IL-1β)及烟碱型乙酰胆碱受体a7信使核糖核酸(nchRa7mRNA)表达的影响,探讨大肠下合穴上巨虚治疗对应腑病是否存在相对特异性。方法将70只健康SD大鼠随机分为空白组、模型组、上巨虚组、足三里组、下巨虚组、阳陵泉组及承筋组,每组10只,雌雄各半。除空白组外均采用2-4-6三硝基苯磺酸/乙醇溶液灌肠诱导建立大鼠溃疡性结肠炎模型,造模成功并治疗10 d后,肉眼观察大鼠结肠黏膜溃疡及炎症情况,ELISA法检测大鼠结肠组织中IL-1b含量,RT-PCR检测nAchRa7mRNA的表达。结果与模型组比,各穴位组结肠损伤有不同程度好转,组织IL-1β含量明显偏低而n ACh Ra7m RNA表达均较高(P<0.05,P<0.01),且上巨虚组、足三里组结肠溃疡评分亦较低(P<0.05,P<0.01);与上巨虚组比,其他4个穴位组结肠n AChRa7mRNA表达均较低(P<0.01),而下巨虚组、阳陵泉组、承筋组结肠溃疡及炎症损伤较严重,结肠溃疡评分及IL-1b含量均偏高(P<0.05,P<0.01)。结论电针治疗溃疡性结肠炎的机制可能是通过影响IL-1β、n Ach Ra7m RNA等调节异常的免疫功能,改善结肠黏膜损伤等来实现的;上巨虚治疗溃疡性结肠炎的总体效应优于足三里、下巨虚、阳陵泉及承筋穴,说明上巨虚穴与对应大肠腑之间存在一定的相对特异性。
