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目的探讨IL-5及嗜酸性粒细胞与人芽囊原虫病患者肠黏膜损伤的关系。方法实验组为确诊为人芽囊原虫感染的30例患者,对照组为30例健康体检者。均做电子肠镜检查,用ELISA法检测肠黏膜组织匀浆中的IL-5水平。实验组取病变黏膜做病理检查,HE染色病理切片,并观察嗜酸性粒细胞的浸润情况。结果经电子肠镜检查,30例人芽囊原虫病患者均出现不同程度的肠道病变,表现为充血、水肿、糜烂、溃疡等。病理学观察病变组织有嗜酸性粒细胞浸润。实验组肠黏膜组织匀浆IL-5(45.75±24.1)pg/ml,对照组为(19.90±7.6)pg/ml,差异有统计学意义(t=5.603 0,P<0.01),且人芽囊原虫感染者肠黏膜组织匀浆IL-5水平随着浸润嗜酸性粒细胞数目增加而逐渐升高,人芽囊原虫感染度与嗜酸性粒细胞浸润数目呈正相关(rs=0.771 1,P<0.01)。结论人芽囊原虫感染能引起患者肠黏膜的病理改变,嗜酸性粒细胞浸润及细胞因子IL-5水平升高。IL-5和嗜酸性粒细胞在人芽囊原虫感染所致的肠黏膜损伤中起重要作用,且IL-5是人芽囊原虫感染引起免疫反应导致肠黏膜损伤的重要细胞因子之一。
Objective To investigate the relationship between IL-5, eosinophils and intestinal mucosal injury in human Blastocystis disease. Methods The experimental group was diagnosed as Blastocystis infection in 30 patients, the control group of 30 healthy subjects. All patients underwent electron colonoscopy. The levels of IL-5 in intestinal mucosa homogenate were detected by ELISA. In the experimental group, lesions were taken for histopathological examination, histopathological sections were stained with HE, and eosinophil infiltration was observed. Results By electron colonoscopy, 30 cases of human Blastocystis disease showed varying degrees of intestinal lesions, manifested as congestion, edema, erosion, ulcers and so on. Pathological observation of eosinophils lesions eosinophil infiltration. The intestinal mucosa homogenate IL-5 (45.75 ± 24.1) pg / ml in the experimental group and (19.90 ± 7.6) pg / ml in the control group were statistically significant (t = 5.603 0, P <0.01) The level of IL-5 in intestinal mucosal tissue homogenate increased gradually with the increase of the number of infiltrating eosinophils, and the positive correlation between the infection degree and the number of eosinophil infiltration (P < 0.01). Conclusions Human Blastocystis infection can cause pathological changes of intestinal mucosa, eosinophil infiltration and cytokines IL-5 levels. IL-5 and eosinophils play an important role in intestinal mucosal injury induced by Blastocystis infection, and IL-5 is one of the important cytokines that causes the immune response to intestinal mucosal injury.