首页> 美国卫生研究院文献>Infection and Immunity >Role of Interleukin-17A in Cell-Mediated Protection against Staphylococcus aureus Infection in Mice Immunized with the Fibrinogen-Binding Domain of Clumping Factor A
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Role of Interleukin-17A in Cell-Mediated Protection against Staphylococcus aureus Infection in Mice Immunized with the Fibrinogen-Binding Domain of Clumping Factor A

机译:白细胞介素17A在细胞介导的抗金黄色葡萄球菌感染的小鼠中的作用该小鼠免疫了集束因子A的纤维蛋白原结合域。

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摘要

Clumping factor A (ClfA) is a fibrinogen-binding cell wall-attached protein and an important virulence factor of Staphylococcus aureus. Previous studies reported that an immunization with the fibrinogen-binding domain of ClfA (ClfA40-559) protected animals against S. aureus infection. It was reported that some cytokines are involved in the pathogenesis of staphylococcal diseases and in host defense against S. aureus infection. However, the role of cytokines in the protective effect of ClfA40-559 as a vaccine has not been elucidated. In this study, we demonstrated that the spleen cells of ClfA40-559-immunized mice produced a large amount of interleukin-17A (IL-17A). The protective effect of immunization was exerted in wild-type mice but not in IL-17A-deficient mice. IL-17A mRNA expression was increased in the spleens and kidneys of immunized mice after infection. CXCL2 and CCL2 mRNA expression was increased in the spleens and kidneys, respectively. Consistent with upregulation of the mRNA expression, neutrophils infiltrated into the spleens extensively and macrophage infiltration was observed in the kidneys of immunized mice. These results suggest that immunization with ClfA40-559 induces the IL-17A-producing cells and that IL-17-mediated cellular immunity is involved in the protective effect induced by immunization with ClfA40-559 against S. aureus infection.
机译:聚集因子A(ClfA)是一种与纤维蛋白原结合的细胞壁附着蛋白,是金黄色葡萄球菌的重要毒力因子。先前的研究报道,用ClfA的纤维蛋白原结合域(ClfA40-559)进行的免疫保护了动物免受金黄色葡萄球菌感染。据报道,某些细胞因子参与葡萄球菌疾病的发病机理和抗金黄色葡萄球菌感染的宿主防御。但是,尚未阐明细胞因子在作为疫苗的ClfA40-559的保护作用中的作用。在这项研究中,我们证明了经ClfA40-559免疫的小鼠的脾细胞产生了大量的白介素17A(IL-17A)。免疫的保护作用在野生型小鼠中发挥,但在IL-17A缺陷型小鼠中不发挥。感染后,免疫小鼠的脾脏和肾脏中IL-17A mRNA表达增加。 CXCL2和CCL2 mRNA表达分别在脾脏和肾脏中增加。与mRNA表达的上调一致,在免疫小鼠的肾脏中,嗜中性粒细胞广泛浸入脾脏并观察到巨噬细胞浸润。这些结果表明,用ClfA40-559免疫诱导了产生IL-17A的细胞,并且IL-17介导的细胞免疫参与了用ClfA40-559免疫金黄色葡萄球菌感染诱导的保护作用。

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