曼氏血吸虫可溶性卵抗原对实验性小鼠糖尿病病程的免疫调节作用

IF 0.6 Q4 PARASITOLOGY
Naglaa S. M. El-Gebaly, M. Rehan, D. Abdelfattah
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引用次数: 2

摘要

背景:众所周知,蠕虫感染,特别是S.mansoni,可诱导对多种自身免疫性疾病的保护作用,包括1型糖尿病(TID)。在非肥胖糖尿病小鼠(NOD)中观察到的S.mansoni对糖尿病发展的显著抑制或延迟,似乎是由于通过IL-10的产生调节糖尿病相关的th1反应对保护性th2反应。目的:研究曼梭菌SEA对诱导的tid小鼠免疫应答的影响。材料与方法:选取体重90 ~ 100g的6周龄雄性瑞士白化小鼠90只,分为5组;对照组(I):链脲佐菌素(STZ)治疗组(II);可溶性蛋抗原(SEA)免疫组(III);(STZ+SEA)组(IV);(SEA+STZ)组(V)。用比色法测定小鼠在第2周和第4周的血糖水平,用酶联免疫吸附试验(ELISA)测定IL-10。五组胰腺切片的组织病理学检查显示胰腺炎症的存在或不存在迹象。结果:显著降低血糖水平分别发生在两组相比组II和III和V在4周组III, IV和V组II相比,第四组V相比组。显著更高的il - 10水平分别发生在两组第四章和第五章与第二组相比,在团体IV和V相比,第三组和第四组V相比组。在4周,显著增加il - 10水平发生在第二组,IV, V组相比,与IV组比较,III组和I组之间无显著差异。ⅰ组和ⅲ组胰腺切片的组织病理学改变显示胰腺细胞结构正常;与STZ同时治疗的II组和IV组在2周时出现朗格汉斯岛空泡化和坏死,IV组炎症消退。V组在两周均出现血管扩张和炎症细胞。结论:mansoni来源的SEA对TID具有保护作用,可改善血糖控制,提示mansoni感染具有保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Immunomodulating effect of Schistosoma mansoni soluble egg antigen on course of induced diabetes mellitus in experimental mice
Background: Helminth infections, particularly S.mansoni, are known to induce a protective role against various forms of autoimmune diseases, including type 1diabetes (TID). The observed S.mansoni significant inhibition or delay of diabetes development in non-obese diabetic mice (NOD), appeared to be due to a modulation of the diabetes-associated th1response towards protective th2 responses through IL-10 production. Objective: To study the effect of S. mansoni SEA on the immune response in induced TIDmouse moduel.  Material and Methods: In this study, 90 male Swiss Albino mice of 6 weeks old, weighing between 90 and 100g were divided into 5 groups; control group (I): Streptozontocin (STZ)-treated group (II); soluble egg antigen (SEA)-immunized group (III); (STZ+SEA) group (IV); (SEA+STZ) group (V). Mice were subjected to measurement of blood glucose levels at two and four weeks by colorimetric method, and measurement of IL-10 by enzyme linked immunosorbent assay (ELISA). Histopathological examination of pancreatic sections of the five groups investigated signs suggesting presence or absence of pancreatic inflammation.   Results: Significant lowering of blood glucose level occurred at 2-weeks in groups III and V compared to group II and at 4-weeks in groups III, IV and V compared to group II, and in group V compared to group IV. Significant higher IL-10 level occurred at 2-weeks in groups IV and V compared to group II, and in groups IV and V compared to group III and in group V compared to group IV. In 4-weeks, significant increase in IL-10 level occurred in groups II, IV, V compared to group I, and in group V compared to group IV. No significant difference between groups III and I was recorded. Histopathological changes of pancreatic sections of groups I and III showed normal architecture of pancreatic cells; While groups II and IV coinciding with STZ treatment showed vacuolation and necrosis of islets of Langerhans at 2-weeks the inflammation subsided in group IV. In group V there was dilation of blood vessels with inflammatory cells at both weeks. Conclusion: S.mansoni derived SEA proved to be protective against TID leading to improvement of blood sugar control and indicating the protective role of S.mansoni infection.
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