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研究伤寒沙门菌质粒pRST98在沙门菌致病中的作用机制。将伤寒沙门菌质粒pRST98导入鼠伤寒沙门菌低毒株RIA形成接合子pRST98/RIA,经腹腔感染小鼠,检测脾脏DC的数量及其表面分子CD80和CD86的表达,比较细菌刺激DC成熟的能力;将接合子的热灭活抗原与其致敏的DC共培养,检测IFN-γ和IL-10水平,评价spv活化DC分泌细胞因子的能力;将接合子致敏的DC分别与初始型CD4+和CD8+T细胞进行混合淋巴细胞反应,检测DC刺激初始型T细胞活化增殖的能力。实验结果表明,pRST98/RIA接合子感染组小鼠脾脏DC的数量及其表面分子的表达均高于对照组(P<0.05),DC分泌的细胞因子水平与对照组无显著性差异(P>0.05),但其刺激初始型T细胞增殖的能力则明显增强(P<0.05)。说明携带pRST98质粒的沙门菌感染能增强DC介导的特异性免疫应答。
To study the role of Salmonella typhi plasmid pRST98 in the pathogenesis of Salmonella. Salmonella typhimurium plasmid pRST98 was introduced into RHA of Salmonella typhimurium to form conjugate pRST98 / RIA. The mice were inoculated intraperitoneally to detect the number of DC and the expression of surface molecules CD80 and CD86. The ability of bacteria to stimulate DC maturation was compared ; Co-cultured with heat-inactivated antigens of the conjugates and their sensitized DCs to detect the levels of IFN-γ and IL-10; evaluate the ability of spv to activate DCs to secrete cytokines; CD8 + T cells were mixed lymphocyte reaction to detect the ability of DC-stimulated naive T cells to proliferate. The experimental results showed that the number of spleen DC and the expression of its surface molecules in pRST98 / RIA conjugate-infected mice were significantly higher than those in control group (P <0.05). The levels of cytokines secreted by DCs in DCs were not significantly different from those in control group (P> 0.05), but its ability to stimulate the proliferation of naive T cells was significantly enhanced (P <0.05). This shows that Salmonella infection carrying pRST98 plasmid can enhance the DC-mediated specific immune response.