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fractalkine减轻产前应激诱导的小胶质细胞活化

Fractalkine Attenuates Microglial Cell Activation Induced by Prenatal Stress.

作者信息

Ślusarczyk Joanna, Trojan Ewa, Głombik Katarzyna, Chamera Katarzyna, Roman Adam, Budziszewska Bogusława, Basta-Kaim Agnieszka

机构信息

Department of Experimental Neuroendocrinology, Institute of Pharmacology, Polish Academy of Sciences, 12 Smętna Street, 31-343 Krakow, Poland.

Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences, 12 Smętna Street, 31-343 Krakow, Poland.

出版信息

Neural Plast. 2016;2016:7258201. doi: 10.1155/2016/7258201. Epub 2016 Apr 27.

DOI:10.1155/2016/7258201
PMID:27239349
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4863104/
Abstract

The potential contribution of inflammation to the development of neuropsychiatric diseases has recently received substantial attention. In the brain, the main immune cells are the microglia. As they are the main source of inflammatory factors, it is plausible that the regulation of their activation may be a potential therapeutic target. Fractalkine (CX3CL1) and its receptor CX3CR1 play a crucial role in the control of the biological activity of the microglia. In the present study, using microglial cultures we investigated whether fractalkine is able to reverse changes in microglia caused by a prenatal stress procedure. Our study found that the microglia do not express fractalkine. Prenatal stress decreases the expression of the fractalkine receptor, which in turn is enhanced by the administration of exogenous fractalkine. Moreover, treatment with fractalkine diminishes the prenatal stress-induced overproduction of proinflammatory factors such as IL-1β, IL-18, IL-6, TNF-α, CCL2, or NO in the microglial cells derived from prenatally stressed newborns. In conclusion, the present results revealed that the pathological activation of microglia in prenatally stressed newborns may be attenuated by fractalkine administration. Therefore, understanding of the role of the CX3CL1-CX3CR1 system may help to elucidate the mechanisms underlying the neuron-microglia interaction and its role in pathological conditions in the brain.

摘要

炎症对神经精神疾病发展的潜在影响最近受到了广泛关注。在大脑中，主要的免疫细胞是小胶质细胞。由于它们是炎症因子的主要来源，因此调节其激活可能是一个潜在的治疗靶点。趋化因子（CX3CL1）及其受体CX3CR1在控制小胶质细胞的生物活性中起着关键作用。在本研究中，我们使用小胶质细胞培养物研究了趋化因子是否能够逆转产前应激程序引起的小胶质细胞变化。我们的研究发现小胶质细胞不表达趋化因子。产前应激会降低趋化因子受体的表达，而外源趋化因子的给药会增强这种表达。此外，用趋化因子治疗可减少产前应激诱导的来自产前应激新生儿的小胶质细胞中促炎因子如IL-1β、IL-18、IL-6、TNF-α、CCL2或NO的过度产生。总之，目前的结果表明，产前应激新生儿中小胶质细胞的病理激活可能通过给予趋化因子而减弱。因此，了解CX3CL1-CX3CRI系统的作用可能有助于阐明神经元-小胶质细胞相互作用的机制及其在大脑病理状况中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/88babb423839/NP2016-7258201.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/6dbc8f1410f6/NP2016-7258201.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/3673b4c4b02c/NP2016-7258201.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/12337a3ee219/NP2016-7258201.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/b5509755b8b3/NP2016-7258201.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/79d89ec6edd8/NP2016-7258201.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/88babb423839/NP2016-7258201.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/6dbc8f1410f6/NP2016-7258201.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/3673b4c4b02c/NP2016-7258201.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/12337a3ee219/NP2016-7258201.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/b5509755b8b3/NP2016-7258201.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/79d89ec6edd8/NP2016-7258201.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb1/4863104/88babb423839/NP2016-7258201.006.jpg

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