霍乱毒素B亚单位和旋毛虫幼虫抗原诱导黏膜免疫结果分析

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目的探讨黏膜佐剂霍乱毒素B 亚单位(CT-B )在激发旋毛虫感染的黏膜免疫中的作用。方法24rrrrrrrrn只NI H 小鼠随机分为4 组,每组6 只。CT-B 免疫组:每只小鼠于0 、7 、14 d 用含幼虫抗原100 μg 、C T-B 10 μg 的免疫原200 μl 经口灌服;正常对照组;免疫后感染组:免疫方法同CT-B 免疫组,末次免疫后第7 天,每只小鼠用200 条旋rrrrrrrrn毛虫进行感染;单纯感染组:不免疫,与免疫后感染组同时进行感染。CT 蛳B 免疫组与正常对照组在免疫后第7 天、免rrrrrrrrn疫后感染组与单纯感染组在感染后第7 天分别取血检测Ig A 、Ig G 1 、Ig G 2 b ,刮取肠黏液检测sIgA ,检测肠道成虫数,并rrrrrrrrn收集每鼠雌虫,在体外检查其生殖力。结果与单纯感染组相比,CT-B 免疫后感染组肠道成虫数明显减少,雌虫生rrrrrrrrn殖力明显降低,成虫与新生幼虫减虫率分别为88.2%和72.4%。CT-B 免疫组小鼠肠黏液sIg A 、血清Ig A 较对照组小rrrrrrrrn鼠明显提高(0 .2 9 ±0 .04 vs 0.09 ±0.02,0.21 ±0.06 vs 0.08 ±0.01,P <0.001);而两组Ig G 1 和Ig G 2 b 水平无显著性差rrrrrrrrn异(P>0.05)。CT-B 免疫后感染组小鼠肠黏液sIg A 、血清Ig A 较单纯感染组小鼠相比有显著性差异(0 .5 5 ±0 .28 vsrrrrrrrrn0.08 ±0.15,0.33 ±0.06 vs 0.10 ±0.10,P <0.001),而 Objective To investigate the role of mucosal adjuvant cholera toxin B subunit (CT-B) in mucosal immunity induced by Trichinella spiralis infection. Methods 24 NI mice were randomly divided into 4 groups with 6 mice in each group. CT-B immunization group: Each mouse was orally administered with 200 microliters of immunogen containing 100 μg of larval antigen and 10 μg of C TB on days 0, 7 and 14; normal control group; immunized group CT-B group, 200 mice were infected with 200 caterpillars on the 7th day after the last immunization. In the simple infection group, Infection with the group after immunization. CT 蛳 B immunization group and the normal control group on the 7th day after immunization, immunization group and infection alone group were 7 days after infection Blood samples were collected for detection of Ig A, Ig G 1, Ig G 2 b, scraping of intestinal mucus to detect sIgA, detection of intestinal tract number, and collection of each mouse Female, examine its fecundity in vitro. Results Compared with the simple infection group, the number of adult worms in CT-B group was significantly decreased, and the fecundity of adult female mice was significantly lower than that in pure infected group Neonatal larval worm reduction rates were 88.2% and 72.4%. CT-B immune mice intestinal mucus sIg A, serum Ig A than the control group was significantly increased (0.29 ± 0. .04 vs. 0.09 ± 0.02,0.21 ± 0.06 vs 0.08 ± 0.01, P <0.001). There was no significant difference in Ig G 1 and Ig G 2 b levels between the two groups Different (P> 0.05). There was a significant difference in sIgA and IgA of intestinal mucus between CT-B group and control group (0.55 ± 0.28 vs 0.55 ± 0.28, r r r n0.08 ± 0.15, 0.33 ± 0.06 vs 0.10 ± 0.10, P <0.001)
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