摘要
目的：为探讨细胞毒素相关蛋白（CagA）与幽门螺杆菌(Hp)相关胃十二指肠疾病的关系及其可能的机制。方法：应用间接ELISA法定性检测170例胃镜受检查者CagAHpIgG抗体，用双抗体夹心ELISA法检测其中76例患者胃粘膜匀浆上清液中的白细胞介素8（IL－8）含量。结果：170例受检者中，Hp感染者106例，其中CagA阳性69例，阳性率为6509% ，Hp感染的DU、GU、GCa患者CagA阳性率明显高于Hp感染的CG患者（P<0.05）, DU、GU、GCa组间无明显差异（P>0．05）;活动性胃炎CagA阳性率与非活动性胃炎相比较无显著性差别（P＞0，05）；血清CagA阳性的Hp感染者胃粘膜IL8含量显著高于CagA阴性者（P<0.05），后者又显著高于非Hp感染者（P<0．005）；活动性胃炎胃粘膜IL－8含量明显高于非活动性胃炎（P<0.05）。结论：CagA与Hp相关的严重胃十二指肠疾病密切相关，其机制可能与CagA介导胃粘膜IL8的产生，后者参与Hp相关性活动性胃炎的病理过程有关。
To investigate the relationship between cy totoxinassociated protein (CagA) and Hpylorirelated gastroduodenal disease a nd study the mechanisms involved in themMethods：The gastric antral mucosal biopsies and serum were obtained from 170 patients,Serum CagA an tibodies were detected by an indirect ELISA assayLevels of interleukin(IL8 ) in the gastric biopsy homogenate supernatant fluid of 76 in 170 patients were measured by a doubleantibody sandwich ELISA assayResults： It was showed that 106 of 170 patients were infected by Hpylori; 69 of 106 Hpylori infected patients were CagA seropositive (65.09%) Serologic recognition o f CagA protein is significantly more frequent in patients who were Hpylori inf ec ted with ulcer disease and gastric cancer than in those with gastritis alone ( P< 0．05),but there was no statistical difference between duodenal bulbar ulcer、ga stric ulcer、gastric cancer groups(P>0.05) Serologic recognition of CagA protein is not more frequent in patients with active gastritis than those with in active gastritis（P>0.05） The mucosal levels of IL8 were significantly higher in CagA seropositive Hpyloriinfected patients than in those CagA n egative patients(P<0.05) and the latter were significantly higher than tho se Hpylorinegative patients(P<0.005)IL8 concentrations were signif icantly higher in active gastritis than in those with inactive gastritis(P<0.05)Conclusion:These results indicated that a clear correla tion exists between CagA and Hpylorirelated severe gastroduodenal diseaseThe mechanisms may involve the ability of a CagA+ Hpylori strains to induce higher tissue levels of IL－8 and IL－8 enhancement of the activity of mucosal i nflammation
