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首页> 外文期刊>Medical Microbiology and Immunology >IL-17A plays an important role in protection induced by vaccination with fibronectin-binding domain of fibronectin-binding protein A against Staphylococcus aureus infection
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IL-17A plays an important role in protection induced by vaccination with fibronectin-binding domain of fibronectin-binding protein A against Staphylococcus aureus infection

机译:IL-17A在用纤维连接蛋白结合蛋白A的纤维连接蛋白结合结构域接种诱导的纤维连接蛋白结合蛋白A抗葡萄球菌感染的保护作用重要作用

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摘要

Fibronectin-binding protein A (FnBPA) of Staphylococcus aureus is a microbial surface component recognizing adhesive matrix molecules and has been known as one of the most important virulence factors involved in the initiation step of S. aureus infection. Therefore, it has been considered as a potential vaccine candidate. Previous studies have reported that vaccination with FnBPA protects animals against S. aureus infection. In this study, we demonstrated that vaccination with fibronectin-binding domain of FnBPA (FnBPA(541-870)) protects wild-type mice but not interleukin-17A (IL-17A)-deficient mice against S. aureus infection. Moderate levels of antigen-specific immunoglobulins were produced in the sera of vaccinated wild-type and IL-17A-deficient mice. The spleen cells of vaccinated mice produced IL-17A by stimulation with the antigen, and IL-17A mRNA expression was increased in the spleens and livers of vaccinated mice after infection. CXCL1 and CXCL2 mRNA expression was increased in the spleens, and myeloperoxidase (MPO) activity in the spleens and livers was increased in the vaccinated mice after infection. These results suggest that vaccination with FnBPA(541-870) induces the IL-17A-producing cells and that IL-17A-mediated cellular immunity is involved in the protective effect on S. aureus infection.
机译:金黄色葡萄球菌的纤连蛋白结合蛋白A(FNBPA)是识别粘合剂基质分子的微生物表面成分,并且已知是S.UUREUS感染引发步骤中涉及的最重要的毒力因子之一。因此,它被认为是潜在的疫苗候选者。以前的研究报告说,与FNBPA的疫苗接种保护动物免受S. aureus感染。在这项研究中,我们证明了具有FnBPA的纤连蛋白结合结构域的疫苗接种(FNBPA(541-870))保护野生型小鼠但不是白细胞介素-17a(IL-17A) - 抗病患者感染。在疫苗的野生型和IL-17A缺陷小鼠的血清中产生适度的抗原特异性免疫球蛋白。接种疫苗的脾细胞通过用抗原刺激产生IL-17a,并且在感染后脾脏和疫苗的小鼠的脾脏和肝脏中增加了IL-17a mRNA表达。 CXCL1和CXCL2 mRNA表达在脾脏中升高,脾脏和肝脏中的髓过氧化物酶(MPO)活性在感染后疫苗的小鼠增加。这些结果表明,使用FNBPA(541-870)的疫苗接种诱导IL-17A产生细胞,并且IL-17A介导的细胞免疫接受对S. aureus感染的保护作用。

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