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在严重脓毒症动物模型中对小胶质细胞表型的特征描述和调控。

Characterization and modulation of microglial phenotypes in an animal model of severe sepsis.

机构信息

Laboratory of Experimental Pathophysiology, Graduate Program in Health Sciences, University of Southern Santa Catarina, Criciúma, SC, Brazil.

Centro de Estudos em Estresse Oxidativo, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.

出版信息

J Cell Mol Med. 2020 Jan;24(1):88-97. doi: 10.1111/jcmm.14606. Epub 2019 Oct 26.

DOI:10.1111/jcmm.14606
PMID:31654493
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6933367/
Abstract

We aim to characterize the kinetics of early and late microglial phenotypes after systemic inflammation in an animal model of severe sepsis and the effects of minocycline on these phenotypes. Rats were subjected to CLP, and some animals were treated with minocycline (10 ug/kg) by i.c.v. administration. Animals were killed 24 hours, 5, 10 and 30 days after sepsis induction, and serum and hippocampus were collected for subsequent analyses. Real-time PCR was performed for M1 and M2 markers. TNF-α, IL-1β, IL-6, IL-10, CCL-22 and nitrite/nitrate levels were measured. Immunofluorescence for IBA-1, CD11b and arginase was also performed. We demonstrated that early after sepsis, there was a preponderant up-regulation of M1 markers, and this was not switched to M2 phenotype markers later on. We found that up-regulation of both M1 and M2 markers co-existed up to 30 days after sepsis induction. In addition, minocycline induced a down-regulation, predominantly, of M1 markers. Our results suggest early activation of M1 microglia that is followed by an overlap of both M1 and M2 phenotypes and that the beneficial effects of minocycline on sepsis-associated brain dysfunction may be related to its effects predominantly on the M1 phenotype.

摘要

我们旨在描述严重脓毒症动物模型中全身炎症后早期和晚期小胶质细胞表型的动力学，以及米诺环素对这些表型的影响。大鼠接受 CLP 手术，部分动物通过脑室内注射给予米诺环素（10μg/kg）。动物在脓毒症诱导后 24 小时、5 天、10 天和 30 天处死，收集血清和海马体进行后续分析。进行实时 PCR 检测 M1 和 M2 标志物。测量 TNF-α、IL-1β、IL-6、IL-10、CCL-22 和亚硝酸盐/硝酸盐水平。还进行了 IBA-1、CD11b 和精氨酸酶的免疫荧光检测。我们表明，在脓毒症早期，M1 标志物的上调占主导地位，随后并未向 M2 表型标志物转换。我们发现，在脓毒症诱导后 30 天内，M1 和 M2 标志物的上调同时存在。此外，米诺环素诱导 M1 标志物下调，主要作用于 M1 表型。我们的研究结果表明，M1 小胶质细胞早期激活，随后是 M1 和 M2 表型的重叠，米诺环素对脓毒症相关脑功能障碍的有益作用可能与其对 M1 表型的主要作用有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c6a/6933367/37e44191f4ce/JCMM-24-88-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c6a/6933367/4fc61e4ad0aa/JCMM-24-88-g001.jpg
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