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激活小鼠小胶质细胞针对卡氏棘阿米巴活性的复杂细胞因子网络。

Complex network of cytokines activating murine microglial cell activity against Acanthamoeba castellani.

作者信息

Benedetto Nunzia, Auriault Claude

机构信息

Institute of Microbiology, Faculty of Medicine and Surgery, Second University of the Studies of Naples, Larghetto Sant' Aniello a Caponapoli 2, 80138 Naples, Italy.

出版信息

Eur Cytokine Netw. 2002 Jul-Sep;13(3):351-7.

Abstract

In the central nervous system, cytokine-primed microglia play a pivotal role in host defence against Acanthamoeba castellani infections. In this study, the effect of rIL-1beta, rIL-6 or rTNF-alpha, combined or not with rIFN-gamma, on A. castellani infection of murine microglia was examined. Priming of microglial cells with either rIL-1beta or rIL-6, in the presence or absence of rIFN-gamma, triggered amebastatic activity, while the treatment of microglia with rTNF-alpha plus rIFN-gamma additively triggered, in a dose-dependent fashion, amebicidal activity. Inasmuch as NGMA affected cytokine-triggered anti-parasitic activity during the priming process, the NO-dependent pathway itself appears not to be directly involved in the anti-amebic capacities. These data suggest that the proinflammatory cytokines IL-1beta, IL-6 or TNF-alpha could trigger anti-microbial activity against A. castellani infection in the brain.

摘要

在中枢神经系统中,细胞因子预激活的小胶质细胞在宿主抵御卡氏棘阿米巴感染中起关键作用。在本研究中,检测了重组白细胞介素-1β(rIL-1β)、重组白细胞介素-6(rIL-6)或重组肿瘤坏死因子-α(rTNF-α)单独或与重组干扰素-γ(rIFN-γ)联合使用对小鼠小胶质细胞感染卡氏棘阿米巴的影响。在有或无rIFN-γ的情况下,用rIL-1β或rIL-6预激活小胶质细胞可引发抑阿米巴活性,而用rTNF-α加rIFN-γ处理小胶质细胞则以剂量依赖方式累加引发杀阿米巴活性。由于N-甲基-D-天冬氨酸(NGMA)在预激活过程中影响细胞因子触发的抗寄生虫活性,一氧化氮(NO)依赖性途径本身似乎并不直接参与抗阿米巴能力。这些数据表明,促炎细胞因子IL-1β、IL-6或TNF-α可触发针对脑内卡氏棘阿米巴感染的抗菌活性。

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