Hp感染儿童胃十二指肠粘膜IL-8及IL-8 mRNA的研究

目的　检测Hp感染儿童胃、十二指肠粘膜中IL 8及IL 8mRNA的变化 ,从蛋白和分子水平探讨Hp对细胞因子IL 8的影响 ,以及IL 8在Hp相关性胃十二指肠疾病中的作用。方法　胃镜下取胃窦及十二指肠粘膜活检标本 ,用ELISA法和RT PCR半定量法测定胃及十二指肠粘膜中IL 8的含量和IL 8mRNA的表达量。结果　Hp阳性者胃粘膜IL 8为 2 4 66～ 177 77pg/mg ,IL 8mRNA为2 3 7～ 4 99;Hp阴性者胃粘膜IL 8为 2 94～ 12 98pg/mg,IL 8mRNA为 0 0 5～ 0 44 ;差异有显著意义(t分别为 12 3 4和 2 9 2 9,P <0 0 1)。Hp阳性者十二指肠粘膜IL 8为 12 98～ 177 77pg/mg ,IL 8mRNA为 1 2 2～ 1 80 ;Hp阴性者十二指肠粘膜IL 8为 2 0 4～ 10 43pg/mg ,IL 8mRNA为 0 0 1～ 0 2 3 ;差异有显著意义 (t分别为 7 18和 3 7 2 0 ,P <0 0 1)。活动性胃炎胃粘膜IL 8为 12 98～ 177 77pg/mg,IL 8mRNA为 0 5 1～ 4 99;非活动性胃炎胃粘膜IL 8为 2 0 4～ 10 43pg/mg,IL 8mRNA为 0 0 1～ 0 44 ;差异有显著意义 (t分别为 10 66和 18 62 ,P <0 0 1)。活动性胃炎十二指肠粘膜IL 8为 5 2 8～ 47 76pg/mg ,IL 8mRNA为 0 2 3～ 1 87;非活动性胃炎十二指肠粘膜IL 8为 3 19～ 8 14pg/mg,IL 8mRNA为0 0 1～ 0 2 0 ;差异有显著意义 (

Levels and mRNA expression of interleukin-8 in gastric and duodenal mucosa of children Infected with Helicobacter pylori

Objective To determine the changes of IL 8 and IL 8 mRNA in gastric and duodenal mucosa of children with Hp infection, to study the effect of Helicobacter pylori (Hp) infection on the expression of IL 8 and IL 8 mRNA, and to evaluate its possible roles in the pathogenesis of gastric and duodenal mucosal inflammation in Hp related gastroduodenal diseases Methods Biopsy specimens were taken from the antral and duodenal mucosa on endoscopy in patients with or without Hp infection, which was diagnosed by urease test and Warshing Starry staining The expression of IL 8 in gastric and duodenal mucosa was determied by ELISA, the expression of IL 8 mRNA was determined by using RT PCR Results Inflammation of gastric antral mucosa was more severe in Hp positive group than in Hp negative group aActive inflammation often existed on the basis of chronic inflammation in Hp positive mucosa, and duodenal mucosa had mild chronic inflammation in Hp positive group Of 17 children who were not infected with Hp, 4 had pathologically normal gastric mucosa and had mild chronic gastritis, one child had an active chronic gastritis Ninteen children were infected with Hpand all had chronic gastritis with signs of active inflammation Gastric and duodenal mucosal IL 8 and IL 8 mRNA were higher in HP infected than in non infected childen (IL 8: in gastric mucosa 24 66-177 77 pg/mg, 2 94-12 98 pg/mg, t =12 34, P <0 01; in duodenal mucosa: 4 28-47 76 pg/mg, 2 04-9 52 pg/mg, t =7 18, P <0 01 IL 8 mRNA: in gastric mucosa 2 37-4 99, 0 05-0 44, t =29 29, P <0 01; in duodenal mucosa 1 22-1 87, 0 01-0 23, t =37 20, P <0 01) Children with active chronic gastritis had higher interleukin 8 levels and IL 8 mRNA expression than those with inactive gastritis (IL 8 in gastric mucosa: 12 98-177 77 pg/mg, 2 04-10 43 pg/mg, t =10 66, P <0 01; in duodenal mucosa: 5 28-47 76 pg/mg, 3 19-8 14 pg/mg, t =6 52, P <0 01 IL 8 mRNA in gastric mucosa: 0 51-4 99, 0 01-0 44, t =18 62, P <0 01; in duodenal mucosa: 0 23-1 87, 0 01-0 20, t =19 10, P <0 01) Conclusion Higher expression of IL 8 and IL 8 mRNA was seen in Hp positive gastric and duodenal mucosa and in active gastritis IL 8 may play an important role in the local gastric and duodenal mucosal inflammatory infiltration with a largenumber of neutrophils when there is Hp infection