FTY720 is a treatment for relapsing remitting multiple sclerosis (MS). It is an analog of sphingosine-1-phosphate (S1P) and targets S1P receptors 1, 3, 4, and 5. Recent reports indicate an association between long-term exposure to FTY720 and cases of cryptococcal infection. Here, we studied the effect of FTY720 and its derivative, BAF312, which only target S1P receptors 1 and 5, in a mouse model of cryptococcal infection. We found that treatment with FTY720, but not with BAF312, led to decreased survival and increased organ burden in mouse cryptococcal granulomas. Both FTY720 and BAF312 caused a profound CD4+ and CD8+ T cell depletion in blood and lungs but only treatment with FTY720 led to cryptococcal reactivation. Treatment with FTY720, but not with BAF312, was associated with disorganization of macrophages and with M2 polarization at the granuloma site. In a cell system, FTY720 decreased phagocytosis and production of reactive oxygen species by macrophages, a phenotype recapitulated in the S1pr3-/- knockout macrophages. Our results suggest that FTY720 reactivates cryptococcosis from the granuloma through a S1P receptor 3-mediated mechanism and support the rationale for development of more-specific receptor modulators for therapeutic use of MS.

译文

:FTY720是一种复发缓解型多发性硬化症(MS)的治疗方法。它是1-磷酸鞘氨醇(S1P)的类似物,靶向S1P受体1、3、4和5。最近的报道表明,长期暴露于FTY720与隐球菌感染病例之间存在关联。在这里,我们研究了仅针对S1P受体1和5的FTY720及其衍生物BAF312在隐球菌感染的小鼠模型中的作用。我们发现,用FTY720而不是BAF312进行治疗会导致小鼠隐球菌肉芽肿存活率降低和器官负担增加。 FTY720和BAF312均可在血液和肺部引起严重的CD4和CD8 T细胞耗竭,但仅FTY720治疗可导致隐球菌再激活。用FTY720而不是BAF312进行的治疗与巨噬细胞的紊乱和肉芽肿部位的M2极化有关。在细胞系统中,FTY720减少了巨噬细胞的吞噬作用和活性氧的产生,巨噬细胞是在S1pr3-/-敲除巨噬细胞中概括的表型。我们的研究结果表明FTY720通过S1P受体3介导的机制从肉芽肿中重新激活隐球菌病,并支持开发更特异性的受体调节剂以用于MS的治疗。

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