Suppr超能文献

布鲁氏菌感染中 Caspase-2 依赖性树突状细胞死亡、成熟和 T 细胞的启动。

Caspase-2-dependent dendritic cell death, maturation, and priming of T cells in response to Brucella abortus infection.

机构信息

Unit for Laboratory Animal Medicine and Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, United States of America.

出版信息

PLoS One. 2012;7(8):e43512. doi: 10.1371/journal.pone.0043512. Epub 2012 Aug 22.

Abstract

Smooth virulent Brucella abortus strain 2308 (S2308) causes zoonotic brucellosis in cattle and humans. Rough B. abortus strain RB51, derived from S2308, is a live attenuated cattle vaccine strain licensed in the USA and many other countries. Our previous report indicated that RB51, but not S2308, induces a caspase-2-dependent apoptotic and necrotic macrophage cell death. Dendritic cells (DCs) are professional antigen presenting cells critical for bridging innate and adaptive immune responses. In contrast to Brucella-infected macrophages, here we report that S2308 induced higher levels of apoptotic and necrotic cell death in wild type bone marrow-derived DCs (WT BMDCs) than RB51. The RB51 and S2308-induced BMDC cell death was regulated by caspase-2, indicated by the minimal cell death in RB51 and S2308-infected BMDCs isolated from caspase-2 knockout mice (Casp2KO BMDCs). More S2308 bacteria were taken up by Casp2KO BMDCs than wild type BMDCs. Higher levels of S2308 and RB51 cells were found in infected Casp2KO BMDCs compared to infected WT BMDCs at different time points. RB51-infected wild type BMDCs were mature and activated as shown by significantly up-regulated expression of CD40, CD80, CD86, MHC-I, and MHC-II. RB51 induced the production of cytokines TNF-α, IL-6, IFN-γ and IL12/IL23p40 in infected BMDCs. RB51-infected WT BMDCs also stimulated the proliferation of CD4(+) and CD8(+) T cells compared to uninfected WT BMDCs. However, the maturation, activation, and cytokine secretion are significantly impaired in Casp2KO BMDCs infected with RB51 or Salmonella (control). S2308-infected WT and Casp2KO BMDCs were not activated and could not induce cytokine production. These results demonstrated that virulent smooth strain S2308 induced more apoptotic and necrotic dendritic cell death than live attenuated rough vaccine strain RB51; however, RB51, but not its parent strain S2308, induced caspase-2-mediated DC maturation, cytokine production, antigen presentation, and T cell priming.

摘要

光滑毒力布鲁氏菌 abortus 株 2308(S2308)在牛和人类中引起动物传染病布鲁氏菌病。粗糙布鲁氏菌 abortus 株 RB51 源自 S2308,是一种在美国和许多其他国家获得许可的活减毒牛用疫苗株。我们之前的报告表明,RB51 而非 S2308 诱导依赖半胱天冬酶-2 的凋亡和坏死巨噬细胞死亡。树突状细胞(DC)是连接先天和适应性免疫反应的关键专业抗原呈递细胞。与布鲁氏菌感染的巨噬细胞不同,在这里我们报告 S2308 诱导野生型骨髓来源的树突状细胞(WT BMDC)比 RB51 更高水平的凋亡和坏死细胞死亡。RB51 和 S2308 诱导的 BMDC 细胞死亡受到半胱天冬酶-2 的调节,这表明 RB51 和 S2308 感染的半胱天冬酶-2 敲除小鼠(Casp2KO BMDC)分离的 BMDC 中的细胞死亡最小。与野生型 BMDC 相比,Casp2KO BMDC 摄取的 S2308 细菌更多。在不同时间点,与感染 WT BMDCs 相比,感染 Casp2KO BMDCs 中发现更高水平的 S2308 和 RB51 细胞。RB51 感染的野生型 BMDC 表现出成熟和激活,如 CD40、CD80、CD86、MHC-I 和 MHC-II 的表达显著上调。RB51 在感染的 BMDC 中诱导 TNF-α、IL-6、IFN-γ 和 IL12/IL23p40 细胞因子的产生。与未感染的 WT BMDC 相比,RB51 感染的 WT BMDC 还刺激 CD4(+)和 CD8(+)T 细胞的增殖。然而,在感染 RB51 或沙门氏菌(对照)的 Casp2KO BMDC 中,成熟、激活和细胞因子分泌显著受损。S2308 感染的 WT 和 Casp2KO BMDCs 未被激活,无法诱导细胞因子产生。这些结果表明,毒力光滑株 S2308 诱导的凋亡和坏死树突状细胞死亡比活减毒株 RB51 更多;然而,RB51 而非其亲本株 S2308 诱导半胱天冬酶-2 介导的 DC 成熟、细胞因子产生、抗原呈递和 T 细胞启动。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac73/3425542/1ae2450b9949/pone.0043512.g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验