摘要
目的探讨机体免疫反应在幽门螺杆菌（Ｈｐ）致病中的作用。方法采用间接ＥＬＩＳＡ法检测了１４９例患者血清中抗ＨｐＩｇＥ，并用改良甲苯胺蓝染色法检测其胃粘膜中肥大细胞（ＭＣ）。结果①Ｈｐ阳性者血清抗ＨｐＩｇＥ含量、阳性率和胃粘膜中ＭＣ总数及脱颗粒比均显著高于Ｈｐ阴性者（Ｐ＜０．０１）；②不同胃部疾病之间血清抗ＨｐＩｇＥ含量、阳性率和胃粘膜中ＭＣ总数及脱颗粒比有显著差异，活动性胃炎显著高于非活动性胃炎和消化性溃疡（Ｐ＜０．０１），中重度胃炎显著高于轻度胃炎（Ｐ＜０．００１）；③血清抗ＨｐＩｇＥ阳性者胃粘膜内ＭＣ总数及脱颗粒比均显著高于抗ＨｐＩｇＥ阴性者（Ｐ＜０．０１），且血清抗ＨｐＩｇＥ含量与胃粘膜内ＭＣ脱颗粒比呈正相关（ｒ＝０．６０，Ｐ＜０．００１）。结论血清抗ＨｐＩｇＥ参与了Ｈｐ的致病过程，其机制可能为刺激ＭＣ脱颗粒，而致胃粘膜损伤。
Objective To study the roles of immune responses in Hp pathogenicity. Methods The IgE to H. pylori in serum was tested with indirect ELISA and the improved toluidine blue pig mentation was used for examining the mast cells( MC) in gastric mucosa of 149 patients. Results ①The content and positive rate of serum IgE to H.pylori (0.66,62.75%),the total number of gastric mucosal MC and its degranulation portion (8.11,47.65%) of patients with H. pylori positive were significantly higher than those with H.pylori negative(0.33,6.38%,4.22,31.32%) ( P < 0 01 ). ②The content and positive rate of serum IgE to H. pylori (0.89,81.82%),the total number of gastric mucosal MC and its degranulation portion (8.73,57.42%) of patients with active gastritis were sig nificantly higher than of those without active gastritis(0.40,13.85%,5.54,35.01%) and with peptic ulcer(0.47,38.78%,6.6,38.06%)( P <0.01),and the content and positive rate of serum IgE to H. pylori (0.89,83.33%), the total number of gastric mucosal MC and its degranulation portion (8.79,57.74%) of patients with moderate and severe gastritis were significantly higher than those with mild gastritis(0.41,17.24%,5.68,35.56%) ( P <0.001), ③The total number of gastric mucosal MC and its degranulation portion ( 8.83, 56.6%) of patients with serum IgE to H. pylori positive were significantly higher than those without serum IgE to H. pylori (5.26,31.01%)( P < 0 01 ),and the content of serum IgE to H. pylori was positively correlated with the MC degranulation portion ( r =0.60, P <0.001). Conclusion Serum IgE to H. pylori was involved in Hp pathogenicity, and its mechanisms might related to stimulate MC degranulation and make gastric mucosa injury.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
1999年第4期342-345,共4页
Chinese Journal of Microbiology and Immunology
基金
江西省自然科学基金
