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Repopulating Microglia Promote Brain Repair in an IL-6-Dependent Manner.
Cell ( IF 64.5 ) Pub Date : 2020-03-05 , DOI: 10.1016/j.cell.2020.02.013
Emily F Willis 1 , Kelli P A MacDonald 2 , Quan H Nguyen 3 , Adahir Labrador Garrido 4 , Ellen R Gillespie 4 , Samuel B R Harley 1 , Perry F Bartlett 5 , Wayne A Schroder 6 , Abi G Yates 7 , Daniel C Anthony 7 , Stefan Rose-John 8 , Marc J Ruitenberg 4 , Jana Vukovic 1
Affiliation  

Cognitive dysfunction and reactive microglia are hallmarks of traumatic brain injury (TBI), yet whether these cells contribute to cognitive deficits and secondary inflammatory pathology remains poorly understood. Here, we show that removal of microglia from the mouse brain has little effect on the outcome of TBI, but inducing the turnover of these cells through either pharmacologic or genetic approaches can yield a neuroprotective microglial phenotype that profoundly aids recovery. The beneficial effects of these repopulating microglia are critically dependent on interleukin-6 (IL-6) trans-signaling via the soluble IL-6 receptor (IL-6R) and robustly support adult neurogenesis, specifically by augmenting the survival of newborn neurons that directly support cognitive function. We conclude that microglia in the mammalian brain can be manipulated to adopt a neuroprotective and pro-regenerative phenotype that can aid repair and alleviate the cognitive deficits arising from brain injury.



中文翻译:

重新填充小胶质细胞以IL-6依赖的方式促进大脑修复。

认知功能障碍和反应性小胶质细胞是创伤性脑损伤(TBI)的标志,但是这些细胞是否促成认知功能障碍和继发性炎症病理仍知之甚少。在这里,我们显示从小鼠脑部清除小胶质细胞对TBI的结果影响不大,但是通过药理或遗传方法诱导这些细胞的更新可以产生神经保护性小胶质细胞表型,可以显着帮助恢复。这些繁殖的小胶质细胞的有益作用严重依赖于白介素6(IL-6)反式通过可溶性IL-6受体(IL-6R)发出信号并强烈支持成人神经发生,特别是通过增加直接支持认知功能的新生神经元的存活率。我们得出的结论是,可以操纵哺乳动物大脑中的小胶质细胞,以采取神经保护性和再生性表型,以帮助修复和减轻因脑损伤而引起的认知缺陷。

更新日期:2020-03-05
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