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首页> 外文期刊>Vaccine >Immunity induced with a Salmonella enterica serovar Enteritidis live vaccine is regulated by Th1-cell-dependent cellular and humoral effector mechanisms in susceptible BALB/c mice
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Immunity induced with a Salmonella enterica serovar Enteritidis live vaccine is regulated by Th1-cell-dependent cellular and humoral effector mechanisms in susceptible BALB/c mice

机译：沙门氏菌肠炎沙门氏菌活疫苗诱导的免疫受到易感BALB / c小鼠Th1细胞依赖性细胞和体液效应机制的调节

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The objective of this study was to characterize the immune response induced by a live attenuated Salmonella Enteritidis (SE; ade(-)/his(-)) vaccine using an intraperitoneal immunization/challenge model in susceptible wild-type and cytokine-deficient BALB/c mice. In wild-type mice, inoculation of the SE live vaccine induced a protective immune response characterized by both cellular (production of interleukin(IL)-12 and interferon(IFN)-gamma, granuloma formation in liver and spleen, DTH response) and humoral effector mechanisms (high antigen-specific IgG2a titers). IL-12- and IL-4-deficient mice were immunized to study the individual roles of Th1 and Th2 cells, respectively. Protective immunity in wild-type mice required inoculation of >5 x 10(3)CFU of the attenuated live SE vaccine strain used. While IL-4-deficient mice developed a protective immune response similar to that found in wild-type mice, it was not possible to induce protective immunity in the highly susceptible IL-12-deficient mice due to severe disease symptoms and death following inoculation of the SE vaccine strain (doses >or=5 x 10(2)CFU were lethal for IL-12-deficient mice). Interestingly, persistence of the vaccine strain was observed in IL-4-deficient mice, indicating a role of IL-4 for clearance which, however, did not interfere with protective immunity. Together, the data indicate that the SE live vaccine activates a cellular and a humoral immune response, which are both regulated by Th1 cells via the secretion of IFN-gamma, whereas Th2 cells did not contribute essentially to the SE live-vaccine-induced immunity.
机译：这项研究的目的是在易感的野生型和细胞因子缺陷型BALB / A中使用腹膜内免疫/攻击模型表征由减毒活肠炎沙门氏菌（SE; ade（-）/ his（-））疫苗诱导的免疫反应。 c只小鼠。在野生型小鼠中，接种SE活疫苗可诱导保护性免疫反应，其特征在于细胞（白介素（IL）-12和干扰素（IFN）-γ的产生，肝和脾肉芽肿的形成，DTH反应）和体液效应器机制（高抗原特异性IgG2a滴度）。免疫IL-12和IL-4缺陷小鼠，分别研究Th1和Th2细胞的个体作用。野生型小鼠的保护性免疫需要接种> 5 x 10（3）CFU的减毒活SE疫苗株。尽管IL-4缺陷型小鼠的保护性免疫反应类似于野生型小鼠，但由于严重的疾病症状和接种后的死亡，不可能在高度易感的IL-12缺陷型小鼠中诱导保护性免疫。 SE疫苗株（对于IL-12缺陷型小鼠，剂量大于或等于5 x 10（2）CFU致死）。有趣的是，在IL-4缺陷型小鼠中观察到了疫苗株的持久性，表明IL-4具有清除作用，但是，IL-4没有干扰保护性免疫。总之，数据表明SE活疫苗激活了细胞免疫和体液免疫反应，两者均受Th1细胞通过分泌IFN-γ的调节，而Th2细胞基本上不促进SE活疫苗诱导的免疫。

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