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首页> 外文期刊>Glia >Microglial Regulation of Immunological and Neuroprotective Functions of Astroglia
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Microglial Regulation of Immunological and Neuroprotective Functions of Astroglia

机译：小胶质细胞对星形胶质细胞的免疫和神经保护功能的调节。

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Microglia and astroglia play critical roles in the development, function, and survival of neurons in the CNS. However, under inflammatory conditions the role of astrogliosis in the inflammatory process and its effects on neurons remains unclear. Here, we used several types of cell cultures treated with the bacterial inflammogen LPS to address these questions. We found that the presence of astroglia reduced inflammation-driven neurotoxicity, suggesting that astrogliosis is principally neuroprotective. Neutralization of supernatant glial cell line-derived neurotrophic factor (GDNF) released from astroglia significantly reduced this neuroprotective effect during inflammation. To determine the immunological role of astroglia, we optimized a highly-enriched astroglial culture protocol and demonstrated that LPS failed to induce the synthesis and release of TNF- and iNOS/NO. Instead we found significant enhancement of TNF- and iNOS expression in highly-enriched astroglial cultures required the presence of 0.5-1% microglia, respectively. Thus suggesting that microglial-astroglial interactions are required for LPS to induce the expression of pro-inflammatory factors and GDNF from astroglia. Specifically, we found that microglia-derived TNF- plays a pivotal role as a paracrine signal to regulate the neuroprotective functions of astrogliosis. Taken together, these findings suggest that astroglia may not possess the ability to directly recognize the innate immune stimuli LPS, but rather depend on crosstalk with microglia to elicit release of neurotrophic factors as a counterbalance to support neuronal survival from the collateral damage generated by activated microglia during neuroinflammation. GLIA 2015;63:118-131
机译：小胶质细胞和星形胶质细胞在中枢神经系统神经元的发育，功能和存活中起着关键作用。然而，在炎性条件下，星形胶质细胞增生在炎性过程中的作用及其对神经元的作用仍不清楚。在这里，我们使用了几种用细菌性炎症原LPS处理过的细胞培养物来解决这些问题。我们发现，星形胶质细胞的存在减少了炎症驱动的神经毒性，表明星形胶质细胞增多症主要是神经保护性的。从星形胶质细胞释放的上清液胶质细胞源性神经营养因子（GDNF）的中和作用大大降低了炎症过程中的这种神经保护作用。为了确定星形胶质细胞的免疫学作用，我们优化了高度富集的星形胶质细胞培养方案，并证明LPS无法诱导TNF-和iNOS / NO的合成和释放。相反，我们发现在高度富集的星形胶质细胞培养物中，分别需要0.5-1％小胶质细胞的存在，才能显着增强TNF-和iNOS的表达。因此提示LPS需要小胶质-星形胶质相互作用来诱导星形胶质细胞促炎因子和GDNF的表达。具体来说，我们发现小胶质细胞源性TNF-作为旁分泌信号来调节星形胶质细胞增多症的神经保护功能起着关键作用。综上所述，这些发现表明，星形胶质细胞可能不具有直接识别先天性免疫刺激LPS的能力，而是依靠与小胶质细胞的串扰来引发神经营养因子的释放，以作为由激活的小胶质细胞产生的附带损害来支持神经元生存的平衡。在神经发炎期间。 GLIA 2015; 63：118-131

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